subject:(keratinocyte)

1. 신, 재영. Immunohistochemical Evaluation and Gene Expression Profiling of Senile Lentigo.

Degree: 2012, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/7582 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012356

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BACKGROUND AND OBJECTIVES: Senile lentigines typically appear as dark brown macules on sun-exposed areas. Histologically, they are characterized by hyperpigmentation in the basal layer of… (more)

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BACKGROUND AND OBJECTIVES: Senile lentigines typically appear as dark brown macules on sun-exposed areas. Histologically, they are characterized by hyperpigmentation in the basal layer of the epidermis, combined with elongation of rete ridges. The molecular pathogenesis underlying the initiation and formation of senile lentigines are not completely understood. The histological and immunohistochemical features that characterize facial senile lentigines and their gene expression profiles were investigated. MATERIAL AND METHODS: For routine and immunohistochemical study, formalin-fixed and paraffin-embedded tissue blocks obtained from 20 Korean patients (1 man, 19 women) were used. Immunohistochemical staining of tyrosinase, NKI/beteb, MITF (microphthalmia-associated transcription factor), Ki67, SFRP2 (secreted frizzled-related protein 2), Wnt-5a, p16 and p53 and computer-assisted image analysis were performed. DNA microarray analysis was carried in one female volunteer with both lentigo and melasma. RESULTS: Histological features of senile lentigo of the face were characterized by epidermal hyperpigmentation due to melanocytic proliferation and activation. Epidermal thickness was increased due to increased size of keratinocytes, rather than the number of keratinocytes. In contrast to lentigo occurring elsewhere, facial lentigo in my series showed flattened epidermis rather than lentiginous epidermal hyperplasia in 80% of cases. NKI/beteb and tyrosinase staining suggests melanocytes are constantly activated throughout the evolution of lentigo. Increased expression of p53 in lesion suggests ultraviolet light irradiation is an important factor for epidermal hyperpigmentation. Wnt signaling pathway-associated factors were partially evident in the lesional skin, indicating possible involvement. The severity of senile lentigines could be correlated with the degree of epidermal hyperplasia and categorized, which was further supported by modulations of proliferation and senescence markers. Differentially expressed genes among the normal skin, lentigo and melasma were identified by Affymetrix gene expression analysis, but the results did not match the outcomes derived from immunohistochemistry. CONCLUSIONS: Senile lentigo is a pigmentary disorder of both melanocytes and keratinocytes, controlled by intricate interactions between epidermal and dermal mesenchymal cells.

연구 배경 및 목적: 노인성 흑색점은 일광 노출 부위에 호발하는 갈색 반점 형태의 색소 침착 질환으로, 고령에서 주로 발생하므로 광노화의 진행을 나타낸다. 현재까지 흑색점의 발생과 진행의 분자생물학적 기전은 명확히 밝혀져 있지 않다. 따라서 본 연구에서는 노인성 흑색점 병변에 대한 면역조직화학적 특성을 밝히고 유전자 발현 양상을 연구하고자 하였다. 재료 및 방법: 노인성 흑색점으로 기 진단된 20명의 파라핀 조직 블록에 대해 tyrosinase, NKI/beteb, MITF (microphthalmia-associated transcription factor), Ki67, SFRP2 (secreted frizzled-related protein 2), Wnt-5a, p16과 p53에 대한 면역조직화학 염색을 시행하였다. 면역조직화학 염색된 조직과 hematoxylin & eosin (H&E) 염색된 조직에 대해 컴퓨터 이미지 분석 및 조사자에 의한 반 정량적 분석을 함께 시행하였다. 노인성 흑색점과 기미를 동시에 가진 1명의 여성 자원자에 대하여 병변 조직의 DNA 마이크로어레이 분석을 시행하였다. 결과: H&E 염색 상에서는 표피 하부의 과색소 침착이 두드러지게 나타났으며 기존 보고에서 흑색점의 특징으로 설명하였던 표피 능선의 곤봉 모양 연장보다 표피가 편평하게 변화한 경우가…

Advisors/Committee Members: 대학원 의학과, 201024243, 신, 재영.

Subjects/Keywords: lentigo; immunohistochemistry; melanocyte; keratinocyte; microarray

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

신, �. (2012). Immunohistochemical Evaluation and Gene Expression Profiling of Senile Lentigo. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/7582 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012356

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

신, 재영. “Immunohistochemical Evaluation and Gene Expression Profiling of Senile Lentigo.” 2012. Thesis, Ajou University. Accessed January 25, 2021. http://repository.ajou.ac.kr/handle/201003/7582 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012356.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

신, 재영. “Immunohistochemical Evaluation and Gene Expression Profiling of Senile Lentigo.” 2012. Web. 25 Jan 2021.

Vancouver:

신 �. Immunohistochemical Evaluation and Gene Expression Profiling of Senile Lentigo. [Internet] [Thesis]. Ajou University; 2012. [cited 2021 Jan 25]. Available from: http://repository.ajou.ac.kr/handle/201003/7582 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012356.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

신 �. Immunohistochemical Evaluation and Gene Expression Profiling of Senile Lentigo. [Thesis]. Ajou University; 2012. Available from: http://repository.ajou.ac.kr/handle/201003/7582 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012356

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester

2. Kuo, I-Hsin. Activation of Epidermal Toll-like Receptor 2 Enhances Tight Junction Function:Implications for Atopic Dermatitis and Skin Barrier Repair.

Degree: PhD, 2013, University of Rochester

URL: http://hdl.handle.net/1802/27274

► Atopic dermatitis (AD) is a Th2-skewed, allergen-driven skin disease characterized by epidermal tight junction (TJ) defects and a propensity for Staphylococcus aureus (S. aureus) skin… (more)

▼ Atopic dermatitis (AD) is a Th2-skewed, allergen-driven skin disease characterized by epidermal tight junction (TJ) defects and a propensity for Staphylococcus aureus (S. aureus) skin infections. One widely held hypothesis is that the leaky epithelial barrier promotes immunologic responsiveness to allergens through the skin. Toll-like receptor (TLR) 2, a key innate receptor responsive to S. aureus, was originally recognized for its antimicrobial actions, but recently it has been shown to regulate intestinal epithelial barrier. We hypothesized that an effective cutaneous innate immune response might also include skin barrier repair. Furthermore, this barrier repair response may be impaired in AD patients. To determine the importance of TLR2 in epidermal barrier function, we used primary human keratinocytes (PHK), discarded human skins and Tlr2-/- mice. The TLR2 agonist increased TJ protein expression and function in PHK and enhanced TJ barrier repair in a murine wound model that mimics the itch-scratch cycle observed in AD patients. Since AD is a Th2-polarized inflammatory disorder, we hypothesized that Th2 cytokines might impair this TLR2-mediated barrier repair function. Th2 cytokines decreased TLR2 protein expression and attenuated TLR2’s barrier repair function in PHK and human epidermis. STAT6VT mice with a hyper-Th2 immune profile had reduced epidermal TLR2 protein expression and impaired TJ barrier recovery in response to TLR2 agonist. Bringing this observation back to human AD, we observed that epidermal TLR2 protein immunoreactivity was significantly reduced in nonlesional and lesional AD skin as compared to nonatopic controls (NA). The intensity of the TLR2 staining inversely correlated with skin barrier integrity and two Th2 biomarkers (serum total IgE levels and circulating eosinophil counts). In summary, TLR2 activation enhances TJ barrier in murine and human epidermis and is an important part of an epidermal wound repair response. Th2 cytokines commonly found in AD skin reduce epidermal TLR2 expression and barrier repair function. Our findings strongly suggest that antagonizing Th2 cytokines in AD patients may restore TLR2-mediated innate immune responses, which will help repair epidermal barrier defects and possibly also eliminate unwanted cutaneous pathogens.

Subjects/Keywords: TLR2; Tight Junction; Atopic Dermatitis; Keratinocyte

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kuo, I. (2013). Activation of Epidermal Toll-like Receptor 2 Enhances Tight Junction Function:Implications for Atopic Dermatitis and Skin Barrier Repair. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/27274

Chicago Manual of Style (16^th Edition):

Kuo, I-Hsin. “Activation of Epidermal Toll-like Receptor 2 Enhances Tight Junction Function:Implications for Atopic Dermatitis and Skin Barrier Repair.” 2013. Doctoral Dissertation, University of Rochester. Accessed January 25, 2021. http://hdl.handle.net/1802/27274.

MLA Handbook (7^th Edition):

Kuo, I-Hsin. “Activation of Epidermal Toll-like Receptor 2 Enhances Tight Junction Function:Implications for Atopic Dermatitis and Skin Barrier Repair.” 2013. Web. 25 Jan 2021.

Vancouver:

Kuo I. Activation of Epidermal Toll-like Receptor 2 Enhances Tight Junction Function:Implications for Atopic Dermatitis and Skin Barrier Repair. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2021 Jan 25]. Available from: http://hdl.handle.net/1802/27274.

Council of Science Editors:

Kuo I. Activation of Epidermal Toll-like Receptor 2 Enhances Tight Junction Function:Implications for Atopic Dermatitis and Skin Barrier Repair. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/27274

Penn State University

3. Smith, Kayla Jo. THE ROLE OF THE ARYL HYDROCARBON RECEPTOR IN MODULATING SKIN AND INTESTINAL EPITHELIAL PHYSIOLOGY.

Degree: 2017, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/13833kjs5049

► Barrier tissues such as the skin and intestine are important for the first line of defense against injury and exposure to potentially harmful toxicants or… (more)

Subjects/Keywords: aryl hydrocarbon receptor; skin; intestine; inflammation; keratinocyte

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Smith, K. J. (2017). THE ROLE OF THE ARYL HYDROCARBON RECEPTOR IN MODULATING SKIN AND INTESTINAL EPITHELIAL PHYSIOLOGY. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/13833kjs5049

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Smith, Kayla Jo. “THE ROLE OF THE ARYL HYDROCARBON RECEPTOR IN MODULATING SKIN AND INTESTINAL EPITHELIAL PHYSIOLOGY.” 2017. Thesis, Penn State University. Accessed January 25, 2021. https://submit-etda.libraries.psu.edu/catalog/13833kjs5049.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Smith, Kayla Jo. “THE ROLE OF THE ARYL HYDROCARBON RECEPTOR IN MODULATING SKIN AND INTESTINAL EPITHELIAL PHYSIOLOGY.” 2017. Web. 25 Jan 2021.

Vancouver:

Smith KJ. THE ROLE OF THE ARYL HYDROCARBON RECEPTOR IN MODULATING SKIN AND INTESTINAL EPITHELIAL PHYSIOLOGY. [Internet] [Thesis]. Penn State University; 2017. [cited 2021 Jan 25]. Available from: https://submit-etda.libraries.psu.edu/catalog/13833kjs5049.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Smith KJ. THE ROLE OF THE ARYL HYDROCARBON RECEPTOR IN MODULATING SKIN AND INTESTINAL EPITHELIAL PHYSIOLOGY. [Thesis]. Penn State University; 2017. Available from: https://submit-etda.libraries.psu.edu/catalog/13833kjs5049

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Texas

4. Alsrhani, Abdullah Falleh. Studies in Trypsin as an Alarm Substance in Zebrafish.

Degree: 2018, University of North Texas

URL: https://digital.library.unt.edu/ark:/67531/metadc1248500/

► Previous studies have shown that fish release alarming substances into the water to alert their kin to escape from danger. In our laboratory, we found… (more)

▼ Previous studies have shown that fish release alarming substances into the water to alert their kin to escape from danger. In our laboratory, we found that zebrafish produce trypsin and release it from their gills into the environment when they are under stress. By placing the zebrafish larvae in the middle of a small tank and then placing trypsin at one end of the tank, we observed that the larvae moved away from the trypsin zone and almost to the opposite end of the tank. This escape response was significant and did not occur in response to the control substances, bovine serum albumin (BSA), Russell's viper venom (RVV), and collagen. Also, previously, we had shown that the trypsin could act via a protease-activated receptor-2 (PAR2) on the surface of the cells. Therefore, we hypothesized that trypsin would induce a change in neuronal activity in the brain via PAR2-mediated signaling in cells on the surface of the fish body. To investigate whether the trypsin-responsive cells were surface cells, we generated a primary cell culture of zebrafish keratinocytes, confirmed these cells' identity by specific marker expression, and then incubated these cells with the calcium indicator Fluo-4 and exposed them to trypsin. By using calcium flux assay in a flow-cytometer, we found that trypsin-treated keratinocytes showed an increase in intracellular calcium release. To test whether PAR2 mediates the escape response to trypsin, we treated larvae with a PAR2 antagonist and showed that the trypsin-initiated escape response was abrogated. Furthermore, par2a mutants with knockdown of par2a by the piggyback knockdown method failed to respond to trypsin. Trypsin treatment of adult fish led to an approximately 2-fold increase in brain c-fos mRNA levels 45 mins after trypsin treatment, suggesting that trypsin signals may have reached the brain, probably via a spinothalamic pathway. Taken together, our results reveal a novel trypsin-initiated escape response in fish. These studies should enhance our understanding of fish communication in general and alarm behavior in particular. Furthermore, since pain receptors in other animals are also PAR2, our finding may be useful in exploring pathways of pain reception. Advisors/Committee Members: Jagadeeswaran, Pudur, Fuchs, Jannon, Benjamin, Robert, Wright, Amanda, Mills, Nathaniel.

Subjects/Keywords: Trypsin; Behavior; Zebrafish; Knockdown; Keratinocyte; and PAR2

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Alsrhani, A. F. (2018). Studies in Trypsin as an Alarm Substance in Zebrafish. (Thesis). University of North Texas. Retrieved from https://digital.library.unt.edu/ark:/67531/metadc1248500/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Alsrhani, Abdullah Falleh. “Studies in Trypsin as an Alarm Substance in Zebrafish.” 2018. Thesis, University of North Texas. Accessed January 25, 2021. https://digital.library.unt.edu/ark:/67531/metadc1248500/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Alsrhani, Abdullah Falleh. “Studies in Trypsin as an Alarm Substance in Zebrafish.” 2018. Web. 25 Jan 2021.

Vancouver:

Alsrhani AF. Studies in Trypsin as an Alarm Substance in Zebrafish. [Internet] [Thesis]. University of North Texas; 2018. [cited 2021 Jan 25]. Available from: https://digital.library.unt.edu/ark:/67531/metadc1248500/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Alsrhani AF. Studies in Trypsin as an Alarm Substance in Zebrafish. [Thesis]. University of North Texas; 2018. Available from: https://digital.library.unt.edu/ark:/67531/metadc1248500/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

5. Shetty, N. Developing methods of measuring and manipulating melanocyte/keratinocyte ratios to inform potential treatment of vitiligo vulgaris.

Degree: PhD, 2020, Canterbury Christ Church University

URL: https://repository.canterbury.ac.uk/item/8wq64/developing-methods-of-measuring-and-manipulating-melanocyte-keratinocyte-ratios-to-inform-potential-treatment-of-vitiligo-vulgaris ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.818071

► Introduction My doctoral work focuses on the disease vitiligo vulgaris. Several treatments already exist however, one totally successful remedy is unavailable. I have focused on… (more)

Subjects/Keywords: Vitiligo vulgaris; Melanocyte–keratinocyte transplantation procedure

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Shetty, N. (2020). Developing methods of measuring and manipulating melanocyte/keratinocyte ratios to inform potential treatment of vitiligo vulgaris. (Doctoral Dissertation). Canterbury Christ Church University. Retrieved from https://repository.canterbury.ac.uk/item/8wq64/developing-methods-of-measuring-and-manipulating-melanocyte-keratinocyte-ratios-to-inform-potential-treatment-of-vitiligo-vulgaris ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.818071

Chicago Manual of Style (16^th Edition):

Shetty, N. “Developing methods of measuring and manipulating melanocyte/keratinocyte ratios to inform potential treatment of vitiligo vulgaris.” 2020. Doctoral Dissertation, Canterbury Christ Church University. Accessed January 25, 2021. https://repository.canterbury.ac.uk/item/8wq64/developing-methods-of-measuring-and-manipulating-melanocyte-keratinocyte-ratios-to-inform-potential-treatment-of-vitiligo-vulgaris ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.818071.

MLA Handbook (7^th Edition):

Shetty, N. “Developing methods of measuring and manipulating melanocyte/keratinocyte ratios to inform potential treatment of vitiligo vulgaris.” 2020. Web. 25 Jan 2021.

Vancouver:

Shetty N. Developing methods of measuring and manipulating melanocyte/keratinocyte ratios to inform potential treatment of vitiligo vulgaris. [Internet] [Doctoral dissertation]. Canterbury Christ Church University; 2020. [cited 2021 Jan 25]. Available from: https://repository.canterbury.ac.uk/item/8wq64/developing-methods-of-measuring-and-manipulating-melanocyte-keratinocyte-ratios-to-inform-potential-treatment-of-vitiligo-vulgaris ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.818071.

Council of Science Editors:

Shetty N. Developing methods of measuring and manipulating melanocyte/keratinocyte ratios to inform potential treatment of vitiligo vulgaris. [Doctoral Dissertation]. Canterbury Christ Church University; 2020. Available from: https://repository.canterbury.ac.uk/item/8wq64/developing-methods-of-measuring-and-manipulating-melanocyte-keratinocyte-ratios-to-inform-potential-treatment-of-vitiligo-vulgaris ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.818071

6. Michopoulou, Anna. Receptor syndecan-1 controls MMP-9 expression during keratinocyte migration : Le récepteur syndecan-1 contrôle l'expression de MMP-9 au cours de la migration des kératinocytes.

Degree: Docteur es, Biologie, 2016, Lyon

URL: http://www.theses.fr/2016LYSE1130

► La phase de l'épithélialisation de la réparation cutanée se déroule en impliquant plusieurs processus dynamiques et interactifs pendant lesquels les kératinocytes migrent, prolifèrent et se… (more)

▼ La phase de l'épithélialisation de la réparation cutanée se déroule en impliquant plusieurs processus dynamiques et interactifs pendant lesquels les kératinocytes migrent, prolifèrent et se différentient afin de reconstruire la fonction de la barrière. La migration des kératinocytes est l'événement qui détermine l'efficacité du processus entier. Le comportement migratoire est contrôlé au même temps au niveau extracellulaire et intracellulaire et dépend d'interactions dynamiques entre les cellules et leur environnement extracellulaire, des facteurs de croissance et des cytokines. Parmi les protéines de la matrice extracellulaire, la laminine 332 est un substrat d'adhésion majeur des kératinocytes qui joue un rôle important au cours de la migration des kératinocytes, travers son domaine LG4/5 localisé à l'extrémité carboxy-terminale de sa chaine a. Des études récentes ont rapporté que l'induction de la migration des kératinocytes par LG4/5 est dépendante des Métalloprotéinases Matricielles pro-migratoires (MMP)-9 et -1 qui jouent des rôles essentiels au cours de la cicatrisation et surtout pendant la ré-épithélialisation. Etant donné que des travaux antérieurs du laboratoire ont montré que le domaine LG4/5 participe à la dynamique du cytosquelette et à la motilité cellulaire au travers de liaisons avec les récepteurs de type de protéoglycanes à heparane sulfate, syndécan-1 et -4 on a regardé l'implication potentielle de ces récepteurs au processus. Afin d'analyser la participation possible des syndecans dans ce processus, nous avons développé une approche de mutagénèse dirigée dans la protéine LG4/5 recombinante pour altérer les sites de liaison aux syndécan-1 ou -4. Notre analyse PCR et nos résultats de zymographie ont révélé une différence du profile d'activation des MMPs en fonction de la mutation produite et donc de la capacité de la protéine à recruter le syndécan-1 ou le syndécan-4, ainsi que le syndécan-1, et pas la syndécan-4, est impliqué dans l'activation de la production de la MMP-9 par LG4/5. Nous avons ensuite confirmé ces résultats en réduisant l'expression du syndécan-1 dans des kératinocytes et on a pu aussi montrer que le traitement avec des cytokines telles que TNFalpha et IL-1beta, connues pour leur capacité d'induire l'activation de la MMP-9, a produit le même résultat dans ce systéme. L'addition de l'héparine dans nos experiences a inhibé l'activation de l'expression de MMP-9 suggerant que les heparanes sulfates dans syndecan-1 sont impliqué au mécanisme. Pour confirmer ces résultats des experiences avec des séries de syndecan-1 mutés sont en cours. Pour conclure, nos résultats montrent pour la première fois un rôle important de syndecan-1 à l'expression de MMP-9 suggérant que sa re-distribution au front des kératinocytes migratoires puisse éventuellement être liée au clivage ou à la dégradation des protéines de la matrice extracellulaire. En plus, nos résultats proposent que le domain LG4/5 de la laminin 332 libéré soit capable d'affecter la balance de l'expression de la MMP-9 lors de la migration… Advisors/Committee Members: Rousselle, Patricia (thesis director).

Subjects/Keywords: MMP-9; Syndecan-1; Keratinocyte; Laminin 332; MMP-9; Syndecan-1; Keratinocyte; Laminin 332; 571.6

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Michopoulou, A. (2016). Receptor syndecan-1 controls MMP-9 expression during keratinocyte migration : Le récepteur syndecan-1 contrôle l'expression de MMP-9 au cours de la migration des kératinocytes. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2016LYSE1130

Chicago Manual of Style (16^th Edition):

Michopoulou, Anna. “Receptor syndecan-1 controls MMP-9 expression during keratinocyte migration : Le récepteur syndecan-1 contrôle l'expression de MMP-9 au cours de la migration des kératinocytes.” 2016. Doctoral Dissertation, Lyon. Accessed January 25, 2021. http://www.theses.fr/2016LYSE1130.

MLA Handbook (7^th Edition):

Michopoulou, Anna. “Receptor syndecan-1 controls MMP-9 expression during keratinocyte migration : Le récepteur syndecan-1 contrôle l'expression de MMP-9 au cours de la migration des kératinocytes.” 2016. Web. 25 Jan 2021.

Vancouver:

Michopoulou A. Receptor syndecan-1 controls MMP-9 expression during keratinocyte migration : Le récepteur syndecan-1 contrôle l'expression de MMP-9 au cours de la migration des kératinocytes. [Internet] [Doctoral dissertation]. Lyon; 2016. [cited 2021 Jan 25]. Available from: http://www.theses.fr/2016LYSE1130.

Council of Science Editors:

Michopoulou A. Receptor syndecan-1 controls MMP-9 expression during keratinocyte migration : Le récepteur syndecan-1 contrôle l'expression de MMP-9 au cours de la migration des kératinocytes. [Doctoral Dissertation]. Lyon; 2016. Available from: http://www.theses.fr/2016LYSE1130

NSYSU

7. You, Huey-Ling. The roles of tumor susceptibility gene 101 in keratinocyte differentiation and chromatin remodeling of p16INK4a promotor.

Degree: PhD, Biological Sciences, 2007, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110107-114213

► Tumor Susceptibility Gene 101, TSG101, exhibits multiple biological functions including the regulation of gene transcription, vesicular trafficking, cellular growth and differentiation. However, the signals involve… (more)

▼ Tumor Susceptibility Gene 101, TSG101, exhibits multiple biological functions including the regulation of gene transcription, vesicular trafficking, cellular growth and differentiation. However, the signals involve in the regulation of TSG101 gene functions are unclear. In this present study, we observed congruous TSG101 up-regulation and the differentiation status of keratinocyte in both human foreskin tissue and reconstructed organotypic skin culture. In addition, we found an essential and downstream role of TSG101 in calcium-induced early keratinocyte differentiation since TSG101 siRNA inhibits this process. Our results also indicate a PKC-dependent mechanism is involved based on the following findings. First, a PKC agonist, TPA up-regulates TSG101 and keratin 10 under low calcium condition. Second, co-treatment of keratinocytes with GF 109203X, a PKC inhibitor, blocks TPA-induced TSG101 and keratin 10 up-regulation. Previous report indicates TSG101 gene exhibits a TATA-less and Sp1-containing promoter. Our analysis further shows that both calcium and TPA stimulate phosphorylation of Sp1 and the corresponding TSG101 wild type promoter activity, but not the activity of Sp1 site mutant TSG101 promoter. The co-treatment with GF 109203X blocks the above effects of calcium and TPA, implying that this is a PKC signaling-dependent process. Taken together, these data suggest a PKC-Sp1 signaling is involved in early differentiation switch of keratinocyte through up-regulation of TSG101. Functional inactivation experiment indicates that tsg101 is a tumor suppressor in mouse model. However, many studies using human tumor specimens or conditional knockout mouse give discrepant and contradictive results. Therefore, the role of TSG101 in human cancer remains illusive. Here we demonstrate an inverse correlation between TSG101 and p16INK4a or acetylated- histone H4 protein expression profiles in human head and neck squamous cell carcinomas (HNSCC) (N=98, p<0.001). Using conditioned human HEp2 cells, we confirm that TSG101 negatively modulates p16INK4a expression. Chromatin immunoprecipitation and the subsequent PCR analysis reveal that TSG101 dose-dependently decreases the amount of acetylated histone H4-associated chromatin on p16INK4a promoter. In addition, TSG101 interacts and colocalizes with HDAC1 and SUMO-1 in the nucleus. Furthermore, TSG101 confers a dose-dependent effect on promoting HDAC1 SUMOylation, hence its activity. Taken together, our data demonstrate for the first time that TSG101 can promote SUMO-1 modification of HDAC1, which impacts on down-regulation of p16INK4a gene expression, providing evidence whereby TSG101 might participate in the epigenetic silencing of p16INK4a during the development of HNSCC. Advisors/Committee Members: Tsan-Zon Liu (chair), Jiin-Tsuey Cheng (committee member), Pei-Jung Lu (chair), Yi-Ren Hong (chair).

Subjects/Keywords: p16INK4a promotor; differentiation; TSG101; keratinocyte

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

You, H. (2007). The roles of tumor susceptibility gene 101 in keratinocyte differentiation and chromatin remodeling of p16INK4a promotor. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110107-114213

Chicago Manual of Style (16^th Edition):

You, Huey-Ling. “The roles of tumor susceptibility gene 101 in keratinocyte differentiation and chromatin remodeling of p16INK4a promotor.” 2007. Doctoral Dissertation, NSYSU. Accessed January 25, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110107-114213.

MLA Handbook (7^th Edition):

You, Huey-Ling. “The roles of tumor susceptibility gene 101 in keratinocyte differentiation and chromatin remodeling of p16INK4a promotor.” 2007. Web. 25 Jan 2021.

Vancouver:

You H. The roles of tumor susceptibility gene 101 in keratinocyte differentiation and chromatin remodeling of p16INK4a promotor. [Internet] [Doctoral dissertation]. NSYSU; 2007. [cited 2021 Jan 25]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110107-114213.

Council of Science Editors:

You H. The roles of tumor susceptibility gene 101 in keratinocyte differentiation and chromatin remodeling of p16INK4a promotor. [Doctoral Dissertation]. NSYSU; 2007. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0110107-114213

8. Daehn, Ilse Sofia. Effect of growth factors on T-lymphocyte induced keratinocyte apoptosis.

Degree: 2007, Flinders University

URL: http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20071215.233705

► Atopic eczema is a T-lymphocyte mediated chronic inflammatory skin disorder. The interaction of CD4+ T-lymphocytes with epidermal keratinocytes results in dysregulated, chronic inflammation and altered barrier function.… (more)

▼ Atopic eczema is a T-lymphocyte mediated chronic inflammatory skin disorder. The interaction of CD4+ T-lymphocytes with epidermal keratinocytes results in dysregulated, chronic inflammation and altered barrier function. T-lymphocyte induced keratinocyte apoptosis has been proposed as a mechanism by which epidermal integrity is impaired in eczema. Apoptosis of keratinocytes is thought to result from Tlymphocyte associated Fas ligand (FasL) binding to the death receptor Fas on keratinocytes. The primary aim of this project was to characterize the induction of keratinocyte apoptosis by T-lymphocytes and address the hypothesis that insulin-like growth factor-I (IGF-1), transforming growth factor [beta]1 (TGF[beta]1) and a milk derived growth factor extract containing TGF[beta] and IGF-I (whey growth factor extract; WGFE) protect keratinocytes from T-lymphocyte mediated apoptosis. To address the aims of this project, an in vitro co-culture model was developed combining T-lymphocytes with keratinocytes. Co-cultures were initially established using human Jurkat T-lymphocytes and human HaCaT keratinocytes with more extensive characterisation undertaken using primary CD4+ T-lymphocytes together with HaCaTs or normal human epidermal keratinocytes (NHEK). Annexin V and propidium iodide staining was established as the primary method for measuring keratinocyte apoptosis with this validated using sodium butyrate a known inducer of apoptosis. Changes in nuclear fragmentation and cell morphology were also examined as a key feature of apoptosis. The involvement of the Fas pathway was investigated by assessing T-lymphocyte FasL expression, keratinocyte Fas expression and downstream caspase activation. Inflammatory cytokines IFN[gamma] and TNF[alpha] were also examined due to their ability to induce Fas expression. Studies performed with T-lymphocytes demonstrated that keratinocyte apoptosis was induced, with this due primarily to direct T-lymphocytes and keratinocytes interactions, rather than soluble mediators in the co-culture milieu. Activated T-lymphocytes were found to have high levels of FasL and to upregulate keratinocyte Fas expression. The increased keratinocyte Fas was associated with increased IFN[gamma] levels in the co-culture media and activation of the caspase cascade. A Fas blocking antibody prevented T-lymphocyte induced keratinocyte apoptosis demonstrating that this was a Fas dependent event. As the primary function of keratinocytes is to terminally differentiate, the differentiation status of the cells induced to undergo apoptosis was examined. It was demonstrated that T-lymphocytes decrease the intensity of ?6 integrin expression by the keratinocytes. This marker identifies undifferentiated basal cells as high expressors of [alpha]6, with cells in the early stages of differentiation pathway found to be low expressors of [alpha]6. Co-staining with Annexin V demonstrated that the apoptotic keratinocytes were low expressors of [alpha]6 and thus cells…

Subjects/Keywords: keratinocyte; apoptosis; eczema; growth factors

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APA (6^th Edition):

Daehn, I. S. (2007). Effect of growth factors on T-lymphocyte induced keratinocyte apoptosis. (Thesis). Flinders University. Retrieved from http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20071215.233705

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Daehn, Ilse Sofia. “Effect of growth factors on T-lymphocyte induced keratinocyte apoptosis.” 2007. Thesis, Flinders University. Accessed January 25, 2021. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20071215.233705.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Daehn, Ilse Sofia. “Effect of growth factors on T-lymphocyte induced keratinocyte apoptosis.” 2007. Web. 25 Jan 2021.

Vancouver:

Daehn IS. Effect of growth factors on T-lymphocyte induced keratinocyte apoptosis. [Internet] [Thesis]. Flinders University; 2007. [cited 2021 Jan 25]. Available from: http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20071215.233705.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Daehn IS. Effect of growth factors on T-lymphocyte induced keratinocyte apoptosis. [Thesis]. Flinders University; 2007. Available from: http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20071215.233705

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

9. Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.

Degree: 博士（歯学）, 2014, Fukuoka Dental College / 福岡歯科大学

URL: http://id.nii.ac.jp/1167/00000003/

►

Transforming growth factor-β1 (TGF-β1) reportedly causes the differentiation of fibroblasts to myofibroblasts during wound healing. We investigated the mechanism underlying the activation of latent TGF-β1… (more)

Subjects/Keywords: keratinocyte; fibroblast; transforming growth factor-β1; αv-integrin; matrix metalloproteinase

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APA (6^th Edition):

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, H. (2014). Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000003/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. “Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.” 2014. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed January 25, 2021. http://id.nii.ac.jp/1167/00000003/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. “Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.” 2014. Web. 25 Jan 2021.

Vancouver:

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa H. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. [cited 2021 Jan 25]. Available from: http://id.nii.ac.jp/1167/00000003/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa H. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. Available from: http://id.nii.ac.jp/1167/00000003/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

10. Hiromatsu, Ryo; Hatta, Mitsutoki; Okamura, Kazuhiko; Sakagami, Ryuji. NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. : NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line.

Degree: 博士（歯学）, 2015, Fukuoka Dental College / 福岡歯科大学

URL: http://id.nii.ac.jp/1167/00000037/

►

BACKGROUND:CLCA was postulated to be a calcium-activated chloride channel accessory protein. Recent reports indicate that CLCA isoforms are likely to be expressed in different layers… (more)

Subjects/Keywords: 転写制御; ケラチノサイト; CLCA; NF-kB; transcriptioal control; keratinocyte

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APA (6^th Edition):

Hiromatsu, Ryo; Hatta, Mitsutoki; Okamura, Kazuhiko; Sakagami, R. (2015). NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. : NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000037/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hiromatsu, Ryo; Hatta, Mitsutoki; Okamura, Kazuhiko; Sakagami, Ryuji. “NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. : NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line.” 2015. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed January 25, 2021. http://id.nii.ac.jp/1167/00000037/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hiromatsu, Ryo; Hatta, Mitsutoki; Okamura, Kazuhiko; Sakagami, Ryuji. “NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. : NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line.” 2015. Web. 25 Jan 2021.

Vancouver:

Hiromatsu, Ryo; Hatta, Mitsutoki; Okamura, Kazuhiko; Sakagami R. NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. : NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2015. [cited 2021 Jan 25]. Available from: http://id.nii.ac.jp/1167/00000037/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hiromatsu, Ryo; Hatta, Mitsutoki; Okamura, Kazuhiko; Sakagami R. NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. : NF-κB-regulated transcriptional control of CLCA in a differentiated mouse keratinocyte line. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2015. Available from: http://id.nii.ac.jp/1167/00000037/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

UCLA

11. Woods, Michael Connely. Cyclin-D1 Modulation of Vitamin-D-Induced Gene Expression in Oral Keratinocytes.

Degree: Oral Biology, 2013, UCLA

URL: http://www.escholarship.org/uc/item/7tq970cn

► Background: Oral cancer is the sixth most frequent cancer worldwide. Ninety percent of the newly diagnosed oral cancers (+400,000/ year) are characterized as squamous cell… (more)

▼ Background: Oral cancer is the sixth most frequent cancer worldwide. Ninety percent of the newly diagnosed oral cancers (+400,000/ year) are characterized as squamous cell carcinomas (SCC). SCC, which develops in the cells of the oral epithelium, is a highly aggressive and destructive cancer with a propensity for invasion of surrounding tissues and recurrence. Consequently, little is known about the preventive factors that modulate the risk of oral carcinogenesis. Recently however, two epidemiological studies investigating the predictive factors of cancer, found their strongest association between low levels of vitamin D and oro-pharyngeal cancer. It is our labs goal to further investigate this matter in a cellular model that parallels human oro-pharyngeal carcinogenesis. Recently, our lab identified a novel interaction between Cyclin D1 and a nuclear hormone receptor that modulates gene expression, known as the vitamin D receptor (VDR). Objectives: The objective of our research is to investigate the effect of vitamin D treatment on human keratinocytes engineered to overexpress an oncogene (Cyclin D1) commonly amplified in SCC. We intend to explore vitamin D's effect by monitoring changes in the localization of key components in both the VDR and Cyclin D1 pathways. Our findings should begin address the question of whether the interaction of Cyclin D1 and VDR has any impact on key components in either pathway. Methods: Transgenic keratinocytes over expressing cyclin D1 (OKF6-D1) will be used to examine the relationship between the VDR and Cyclin D1 pathways. Immuno-staining of key pathway components will be used to localize these components to nuclear or cytoplasmic compartments that can be visualized by immunofluorescence (IF) . Lastly, western blot analysis of fractionated lysates (cytoplasmic and nuclear) from transgenic and control keratinocytes will be used to confirm any IF findings . Results: Immunohistochemistry points toward a difference in the localization of VDR when transgenic cells are ligand treated. Lastly, reduced levels of VDRs heterodimeric partner (RXR) were identified when transgenic keratinocytes were treated with vitamin D.

Subjects/Keywords: Oncology; Dentistry; Cancer; Cyclin D1; Keratinocyte; Oral; vitamin D

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APA (6^th Edition):

Woods, M. C. (2013). Cyclin-D1 Modulation of Vitamin-D-Induced Gene Expression in Oral Keratinocytes. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/7tq970cn

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Woods, Michael Connely. “Cyclin-D1 Modulation of Vitamin-D-Induced Gene Expression in Oral Keratinocytes.” 2013. Thesis, UCLA. Accessed January 25, 2021. http://www.escholarship.org/uc/item/7tq970cn.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Woods, Michael Connely. “Cyclin-D1 Modulation of Vitamin-D-Induced Gene Expression in Oral Keratinocytes.” 2013. Web. 25 Jan 2021.

Vancouver:

Woods MC. Cyclin-D1 Modulation of Vitamin-D-Induced Gene Expression in Oral Keratinocytes. [Internet] [Thesis]. UCLA; 2013. [cited 2021 Jan 25]. Available from: http://www.escholarship.org/uc/item/7tq970cn.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Woods MC. Cyclin-D1 Modulation of Vitamin-D-Induced Gene Expression in Oral Keratinocytes. [Thesis]. UCLA; 2013. Available from: http://www.escholarship.org/uc/item/7tq970cn

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

12. Bodily, Jason Matthew. THE DIFFERENTIATION-DEPENDENT P742 PROMOTER AND THE HPV31 LIFE CYCLE .

Degree: 2008, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/6506

► Human papillomaviruses (HPVs) are small circular DNA viruses that persistently infect stratified squamous epithelia. HPVs are implicated in the etiology of a wide variety of… (more)

▼ Human papillomaviruses (HPVs) are small circular DNA viruses that persistently infect stratified squamous epithelia. HPVs are implicated in the etiology of a wide variety of hyperproliferative lesions, and particularly in cancer of the cervix. Although much effort has been made to understand the mechanisms by which these agents can lead to the development of malignant carcinomas, much less is understood about the normal life cycle of HPVs. It is clear that all of the major life cycle events of HPV are tied to the differentiation of keratinocyte host cells, including transcription, splicing, translation, replication, virion morphogenesis, and shedding. As a step towards understanding the normal life cycle of HPVs, we have undertaken studies of the differentiation-dependent “late” promoter, p742. Transcripts from this promoter become very abundant upon differentiation of the host cell. We have mapped the core p742 promoter to a 150 base pair region in the E7 ORF and demonstrated that E6/E7 ORF region contains several positive and negative transcriptional elements, including at least one element that acts on the upstream promoter p99. We have found that several differentiation-related transcription factors, including CDP, Skn-1a, and Tst-1 can repress transcriptional activity from p742. The major differentiation response elements appear to reside in the area of the multiple start sites, and enhancer elements in the viral upstream regulatory region contribute to both basal and differentiation-dependent p742 activity. The viral transcription factor E2 does not appear to regulate this promoter. Using several techniques, we have discovered that productive viral genome replication, which is also differentiation dependent, is neither necessary nor sufficient for p742 activation. Finally, we showed that p742 requires the PKCd signaling pathway, and replication requires tyrosine kinases and several of the PKC isoforms. These studies shed light on the elements in the virus genome responsible for late promoter activity, the interaction between differentiation-dependent viral processes, and the signaling pathways in a differentiating cell to which the virus responds. Advisors/Committee Members: Craig Matthew Meyers, Committee Chair/Co-Chair, David Joseph Spector, Committee Member, Richard John Frisque, Committee Member, Neil David Christensen, Committee Member.

Subjects/Keywords: papillomaviruses; transcription; keratinocyte; differentiation; replication

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APA (6^th Edition):

Bodily, J. M. (2008). THE DIFFERENTIATION-DEPENDENT P742 PROMOTER AND THE HPV31 LIFE CYCLE . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/6506

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bodily, Jason Matthew. “THE DIFFERENTIATION-DEPENDENT P742 PROMOTER AND THE HPV31 LIFE CYCLE .” 2008. Thesis, Penn State University. Accessed January 25, 2021. https://submit-etda.libraries.psu.edu/catalog/6506.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bodily, Jason Matthew. “THE DIFFERENTIATION-DEPENDENT P742 PROMOTER AND THE HPV31 LIFE CYCLE .” 2008. Web. 25 Jan 2021.

Vancouver:

Bodily JM. THE DIFFERENTIATION-DEPENDENT P742 PROMOTER AND THE HPV31 LIFE CYCLE . [Internet] [Thesis]. Penn State University; 2008. [cited 2021 Jan 25]. Available from: https://submit-etda.libraries.psu.edu/catalog/6506.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bodily JM. THE DIFFERENTIATION-DEPENDENT P742 PROMOTER AND THE HPV31 LIFE CYCLE . [Thesis]. Penn State University; 2008. Available from: https://submit-etda.libraries.psu.edu/catalog/6506

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of KwaZulu-Natal

13. Jadoo, Sasha. The development of a stratified keratinocyte model for chlamydia trachomatis pathogenesis studies.

Degree: 2017, University of KwaZulu-Natal

URL: https://researchspace.ukzn.ac.za/handle/10413/18370

► A number of different methods to generate stratified keratinocyte layers have been published. These involved the use of normal human epidermal keratinocytes (NHEKs/NEKS), which have… (more)

▼ A number of different methods to generate stratified keratinocyte layers have been published. These involved the use of normal human epidermal keratinocytes (NHEKs/NEKS), which have a better ability to stratify compared to HaCaT keratinocytes, which usually require supplemented growth factors or stromal interactions with fibroblasts to do so. This study aimed to generate a model of stratified keratinocytes, closely resembling in vivo skin, using HaCaT cells and to demonstrate the effect that C. trachomatis has on these layered keratinocytes, allowing us to gain insight on the pathophysiology of this organism. All cells and bacteria were propagated and titrated according to conventional protocols. HaCaT cells were subcultured upon confluence, seeded (1x106 cells/ml) onto collagen-coated PTFE Transwell membrane inserts and incubated at 33°C and 37°C for 24 days to allow differentiation and stratification. Once cells became confluent they were exposed to the air-liquid interface and fed with KGM Gold (Lonza) supplemented with 10% FBS and additional calcium. Thereafter, cells were fixed in 3.7% phosphate-buffered formaldehyde, embedded in a paraffin block, sectioned, stained and viewed. Hematoxylin and Eosin (H&E) staining was used to determine the resemblance to in vivo human skin. Immunofluorescence was used to detect keratin 10, keratin 14 and involucrin which are markers of keratinocyte differentiation. Stratified keratinocyte layers were infected with C. trachomatis and this was confirmed using the MicroTrak ® C. trachomatis Culture Confirmation Test Kit. Subsequent changes to the layers were also observed and recorded. It was shown that HaCaT cells grown at the air-liquid interface on collagen-coated PTFE Transwell membrane inserts were able to stratify at 33°C. However, more layers of keratinocytes were seen at 37°C after the same duration of incubation (24 days). Keratin 10, keratin 14 and involucrin were all detected in the layers grown at both temperatures, suggesting that the keratinocytes had committed to differentiation. However, the fluorescence seen at 33°C for keratin 10 and involucrin was more intense as compared to that seen at 37°. This suggests that although stratification was faster at 37°C, differentiation was quicker at 33°C. C. trachomatis was able to infect layered keratinocytes grown at both temperatures although not all layers formed at 33°C were infected. Degradation of keratinocyte layers after infection with C. trachomatis was more prominent in those grown at 37°C, which is in keeping with previous findings that the optimum growth temperature of the C. trachomatis LGV biovar is 37°C. This study provided a novel insight in suggesting the manner in which C. trachomatis is able to infect and migrate through in vivo skin, leaving room for further studies in which similar methods of generating stratified keratinocytes may be used to better understand the pathophysiology of various other organisms that affect keratinocytes. Advisors/Committee Members: Sturm, Adriaan Willem. (advisor), Joubert, Bronwyn C. (advisor).

Subjects/Keywords: Chlamydia trachomatis.; Lymphogranuloma venereum.; Keratinocytes.; Stratified keratinocyte model.

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APA (6^th Edition):

Jadoo, S. (2017). The development of a stratified keratinocyte model for chlamydia trachomatis pathogenesis studies. (Thesis). University of KwaZulu-Natal. Retrieved from https://researchspace.ukzn.ac.za/handle/10413/18370

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Jadoo, Sasha. “The development of a stratified keratinocyte model for chlamydia trachomatis pathogenesis studies.” 2017. Thesis, University of KwaZulu-Natal. Accessed January 25, 2021. https://researchspace.ukzn.ac.za/handle/10413/18370.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Jadoo, Sasha. “The development of a stratified keratinocyte model for chlamydia trachomatis pathogenesis studies.” 2017. Web. 25 Jan 2021.

Vancouver:

Jadoo S. The development of a stratified keratinocyte model for chlamydia trachomatis pathogenesis studies. [Internet] [Thesis]. University of KwaZulu-Natal; 2017. [cited 2021 Jan 25]. Available from: https://researchspace.ukzn.ac.za/handle/10413/18370.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Jadoo S. The development of a stratified keratinocyte model for chlamydia trachomatis pathogenesis studies. [Thesis]. University of KwaZulu-Natal; 2017. Available from: https://researchspace.ukzn.ac.za/handle/10413/18370

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Illinois – Chicago

14. Chastkofsky, Michael I. The Role of Protein Tyrosine Kinase 6 in UVB-Induced Signaling and Skin Carcinogenesis.

Degree: 2015, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/19403

► Protein Tyrosine Kinase 6 (PTK6) belongs to a small family of Src-related nonmyristoylated intracellular tyrosine kinases and is involved in normal epithelial homeostasis and cancer.… (more)

Subjects/Keywords: PTK6; SIK; BRK; Skin; UVB; Keratinocyte; SCC; Cancer; STAT3; FAK; BCAR1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chastkofsky, M. I. (2015). The Role of Protein Tyrosine Kinase 6 in UVB-Induced Signaling and Skin Carcinogenesis. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/19403

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chastkofsky, Michael I. “The Role of Protein Tyrosine Kinase 6 in UVB-Induced Signaling and Skin Carcinogenesis.” 2015. Thesis, University of Illinois – Chicago. Accessed January 25, 2021. http://hdl.handle.net/10027/19403.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chastkofsky, Michael I. “The Role of Protein Tyrosine Kinase 6 in UVB-Induced Signaling and Skin Carcinogenesis.” 2015. Web. 25 Jan 2021.

Vancouver:

Chastkofsky MI. The Role of Protein Tyrosine Kinase 6 in UVB-Induced Signaling and Skin Carcinogenesis. [Internet] [Thesis]. University of Illinois – Chicago; 2015. [cited 2021 Jan 25]. Available from: http://hdl.handle.net/10027/19403.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chastkofsky MI. The Role of Protein Tyrosine Kinase 6 in UVB-Induced Signaling and Skin Carcinogenesis. [Thesis]. University of Illinois – Chicago; 2015. Available from: http://hdl.handle.net/10027/19403

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

15. 鎌口, 真由美. The differences of collagen XVII between the oral mucosa and the skin discover the pathogenesis of oral lesions in pemphigoid.

Degree: 博士(歯学), 歯学, 2019, Hokkaido University

URL: http://hdl.handle.net/2115/76953

► The basement membrane zone (BMZ) consists of multiple components, including collagen XVII (COL17), which is the major targeted antigen of pemphigoid diseases such as bullous… (more)

▼ The basement membrane zone (BMZ) consists of multiple components, including collagen XVII (COL17), which is the major targeted antigen of pemphigoid diseases such as bullous pemphigoid (BP) and mucous membrane pemphigoid (MMP). The blistering mechanisms in pemphigoid have not been fully elucidated, especially in MMP, which mainly affects the mucosa. No research has addressed the differences in BMZ components between the skin and the oral mucosa. In this study, we investigate the differences of BMZ proteins especially COL17 between the skin and the oral mucosa to elucidate the pathogenesis of oral lesion in pemphigoid. We showed that the MMP sera react preferentially to the oral mucosal substrates than the skin substrates. As well as the diversity of the reactivity of MMP autoantibodies, it was suggested that there are certain differences between the skin and the oral mucosa as autoantigens itself. We found that the expression levels of COL17 were significantly higher in normal human oral mucosal keratinocytes (NHOMKs) than in normal human epidermal keratinocytes (NHEKs). The high expression levels of COL17 compensate for COL17-depletion induced by pemphigoid IgG. These results may influence the clinical differences in pemphigoid. Furthermore, using immunoprecipitation, we revealed that COL17 directly binds to collagen IV (COL4) in NHEKs and NHOMKs. In particular, the C-terminus of COL17 is binding site to COL4 in NHOMKs. MMP-IgG or monoclonal antibody recognizing the C-terminus hindered the interaction of COL17 with COL4 in NHOMKs. These results are clinically relevant to less inflammatory phenotype in MMP. The inflammatory infiltrates around perilesions were significantly less in MMP compared to BP. These results indicate that pemphigoid IgG targeting the C-terminus plays a pathogenic role in blister formation in the oral mucosa to inhibit protein interactions with less inflammation. Advisors/Committee Members: 北川, 善政, 鄭, 漢忠, 樋田, 京子, 岩田, 浩明.

Subjects/Keywords: keratinocyte; collagen XVII; oral mucosa; bullous pemphigoid; depletion

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

鎌口, �. (2019). The differences of collagen XVII between the oral mucosa and the skin discover the pathogenesis of oral lesions in pemphigoid. (Doctoral Dissertation). Hokkaido University. Retrieved from http://hdl.handle.net/2115/76953

Chicago Manual of Style (16^th Edition):

鎌口, 真由美. “The differences of collagen XVII between the oral mucosa and the skin discover the pathogenesis of oral lesions in pemphigoid.” 2019. Doctoral Dissertation, Hokkaido University. Accessed January 25, 2021. http://hdl.handle.net/2115/76953.

MLA Handbook (7^th Edition):

鎌口, 真由美. “The differences of collagen XVII between the oral mucosa and the skin discover the pathogenesis of oral lesions in pemphigoid.” 2019. Web. 25 Jan 2021.

Vancouver:

鎌口 �. The differences of collagen XVII between the oral mucosa and the skin discover the pathogenesis of oral lesions in pemphigoid. [Internet] [Doctoral dissertation]. Hokkaido University; 2019. [cited 2021 Jan 25]. Available from: http://hdl.handle.net/2115/76953.

Council of Science Editors:

鎌口 �. The differences of collagen XVII between the oral mucosa and the skin discover the pathogenesis of oral lesions in pemphigoid. [Doctoral Dissertation]. Hokkaido University; 2019. Available from: http://hdl.handle.net/2115/76953

University of Bradford

16. Lewis, Christopher John. The role of bone morphogenetic protein signalling in the control of skin repair after wounding : cellular and molecular mechanisms of cutaneous wound healing mediated by bone morphogenetic proteins and their antagonist Noggin.

Degree: PhD, 2013, University of Bradford

URL: http://hdl.handle.net/10454/7337

► Bone morphogenetic proteins (BMPs) and their receptors (BMPRs) coordinate tissue development and postnatal remodelling by regulating proliferation, differentiation and apoptosis. However, their role in wound… (more)

Subjects/Keywords: 617.1; Wound healing, Bone morphogenetic protein (BMP), Skin, Keratinocyte, Noggin, Smad

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lewis, C. J. (2013). The role of bone morphogenetic protein signalling in the control of skin repair after wounding : cellular and molecular mechanisms of cutaneous wound healing mediated by bone morphogenetic proteins and their antagonist Noggin. (Doctoral Dissertation). University of Bradford. Retrieved from http://hdl.handle.net/10454/7337

Chicago Manual of Style (16^th Edition):

Lewis, Christopher John. “The role of bone morphogenetic protein signalling in the control of skin repair after wounding : cellular and molecular mechanisms of cutaneous wound healing mediated by bone morphogenetic proteins and their antagonist Noggin.” 2013. Doctoral Dissertation, University of Bradford. Accessed January 25, 2021. http://hdl.handle.net/10454/7337.

MLA Handbook (7^th Edition):

Lewis, Christopher John. “The role of bone morphogenetic protein signalling in the control of skin repair after wounding : cellular and molecular mechanisms of cutaneous wound healing mediated by bone morphogenetic proteins and their antagonist Noggin.” 2013. Web. 25 Jan 2021.

Vancouver:

Lewis CJ. The role of bone morphogenetic protein signalling in the control of skin repair after wounding : cellular and molecular mechanisms of cutaneous wound healing mediated by bone morphogenetic proteins and their antagonist Noggin. [Internet] [Doctoral dissertation]. University of Bradford; 2013. [cited 2021 Jan 25]. Available from: http://hdl.handle.net/10454/7337.

Council of Science Editors:

Lewis CJ. The role of bone morphogenetic protein signalling in the control of skin repair after wounding : cellular and molecular mechanisms of cutaneous wound healing mediated by bone morphogenetic proteins and their antagonist Noggin. [Doctoral Dissertation]. University of Bradford; 2013. Available from: http://hdl.handle.net/10454/7337

University of Western Ontario

17. Ableser, Mark J. Cx43 Reduces Melanoma Growth Within a Keratinocyte Microenvironment and During Tumorigenesis in vivo.

Degree: 2013, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/1473

► Connexins have been frequently identified as tumor suppressors in many cancers, however, their role in melanoma tumorigenesis remains controversial. Here, we show that B16-BL6 mouse… (more)

Subjects/Keywords: Connexin43; Connexin26; Melanoma; Tumorigenesis; Keratinocyte; BL6 Mouse Melanoma Cells; Cancer Biology

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APA (6^th Edition):

Ableser, M. J. (2013). Cx43 Reduces Melanoma Growth Within a Keratinocyte Microenvironment and During Tumorigenesis in vivo. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/1473

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ableser, Mark J. “Cx43 Reduces Melanoma Growth Within a Keratinocyte Microenvironment and During Tumorigenesis in vivo.” 2013. Thesis, University of Western Ontario. Accessed January 25, 2021. https://ir.lib.uwo.ca/etd/1473.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ableser, Mark J. “Cx43 Reduces Melanoma Growth Within a Keratinocyte Microenvironment and During Tumorigenesis in vivo.” 2013. Web. 25 Jan 2021.

Vancouver:

Ableser MJ. Cx43 Reduces Melanoma Growth Within a Keratinocyte Microenvironment and During Tumorigenesis in vivo. [Internet] [Thesis]. University of Western Ontario; 2013. [cited 2021 Jan 25]. Available from: https://ir.lib.uwo.ca/etd/1473.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ableser MJ. Cx43 Reduces Melanoma Growth Within a Keratinocyte Microenvironment and During Tumorigenesis in vivo. [Thesis]. University of Western Ontario; 2013. Available from: https://ir.lib.uwo.ca/etd/1473

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. KOH MEI LING, ROSITA. EFFECTS OF THE TISSUE CULTURE ENVIRONMENT ON HUMAN PRIMARY KERATINOCYTES.

Degree: 2014, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/119453

Subjects/Keywords: Keratinocyte; Culture; Epigenetic Regulation; Oxygen

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

KOH MEI LING, R. (2014). EFFECTS OF THE TISSUE CULTURE ENVIRONMENT ON HUMAN PRIMARY KERATINOCYTES. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/119453

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

KOH MEI LING, ROSITA. “EFFECTS OF THE TISSUE CULTURE ENVIRONMENT ON HUMAN PRIMARY KERATINOCYTES.” 2014. Thesis, National University of Singapore. Accessed January 25, 2021. http://scholarbank.nus.edu.sg/handle/10635/119453.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

KOH MEI LING, ROSITA. “EFFECTS OF THE TISSUE CULTURE ENVIRONMENT ON HUMAN PRIMARY KERATINOCYTES.” 2014. Web. 25 Jan 2021.

Vancouver:

KOH MEI LING R. EFFECTS OF THE TISSUE CULTURE ENVIRONMENT ON HUMAN PRIMARY KERATINOCYTES. [Internet] [Thesis]. National University of Singapore; 2014. [cited 2021 Jan 25]. Available from: http://scholarbank.nus.edu.sg/handle/10635/119453.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

KOH MEI LING R. EFFECTS OF THE TISSUE CULTURE ENVIRONMENT ON HUMAN PRIMARY KERATINOCYTES. [Thesis]. National University of Singapore; 2014. Available from: http://scholarbank.nus.edu.sg/handle/10635/119453

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

19. Clement, Amanda Lynn. Engineering the Keratinocyte Microenvironment: Harnessing Topography to Direct Cellular Function.

Degree: PhD, 2015, Worcester Polytechnic Institute

URL: etd-011215-151605 ; https://digitalcommons.wpi.edu/etd-dissertations/23

► Skin wound healing presents a challenging and expensive clinical problem with nearly 20 million wounds requiring intervention leading to an annual cost of more than… (more)

▼ Skin wound healing presents a challenging and expensive clinical problem with nearly 20 million wounds requiring intervention leading to an annual cost of more than $8 million. Tissue engineered skin substitutes are valuable not only as a clinical therapy for chronic wounds and severe traumas, but also as in vitro 3D model systems to investigate wound healing and skin pathogenesis. However, these substitutes are limited by a lack of topography at the dermal-epidermal junction (DEJ). In contrast, the native DEJ is characterized by a series of dermal papillae which project upward into the epidermal layer and create physical topographic microniches that support keratinocyte stem cell clustering. In this thesis, we created novel 3D skin model systems to investigate the role of microtopography in regulating keratinocyte function and cell fate using scaffolds containing precisely engineered topographic features. We hypothesized that the microtopography of the DEJ creates distinct keratinocyte microniches that promote epidermal morphogenesis and modulate keratinocyte stem cell clustering which can be harnessed to create a more robust skin substitute that expedites wound closure. Using photolithographic techniques, we created micropatterned DEJ analogs and micropatterned dermal-epidermal regeneration matrices (ÂµDERM) which couple a dermal support matrix to a micropatterned DEJ analog. We found that the incorporation of microtopography into our in vitro skin model resulted in a thicker, more robust epidermal layer. Additionally, we identified three distinct functional keratinocyte niches: the proliferative niche in narrow channels, the synthetic niche in wide channels and the keratinocyte stem cell niche in narrow channels and corner topographies. Ultimately, incorporation of both narrow and wide channels on a single construct allowed us to recreate native keratinocyte stem cell patterning in vitro. These model systems will allow us to investigate the role of cellular microniches in regulating cellular function and epidermal disease pathogenesis as well as to identify topographic cues that enhance the rate of wound healing. Advisors/Committee Members: Stelios T. Andreadis, Committee Member, Anjana Jain, Committee Member, Tanja Dominko, Committee Member, Joseph B. Duffy, Committee Member, George D. Pins, Advisor.

Subjects/Keywords: microtopography; keratinocyte function; tissue engineered skin; dermal-epidermal junction

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Clement, A. L. (2015). Engineering the Keratinocyte Microenvironment: Harnessing Topography to Direct Cellular Function. (Doctoral Dissertation). Worcester Polytechnic Institute. Retrieved from etd-011215-151605 ; https://digitalcommons.wpi.edu/etd-dissertations/23

Chicago Manual of Style (16^th Edition):

Clement, Amanda Lynn. “Engineering the Keratinocyte Microenvironment: Harnessing Topography to Direct Cellular Function.” 2015. Doctoral Dissertation, Worcester Polytechnic Institute. Accessed January 25, 2021. etd-011215-151605 ; https://digitalcommons.wpi.edu/etd-dissertations/23.

MLA Handbook (7^th Edition):

Clement, Amanda Lynn. “Engineering the Keratinocyte Microenvironment: Harnessing Topography to Direct Cellular Function.” 2015. Web. 25 Jan 2021.

Vancouver:

Clement AL. Engineering the Keratinocyte Microenvironment: Harnessing Topography to Direct Cellular Function. [Internet] [Doctoral dissertation]. Worcester Polytechnic Institute; 2015. [cited 2021 Jan 25]. Available from: etd-011215-151605 ; https://digitalcommons.wpi.edu/etd-dissertations/23.

Council of Science Editors:

Clement AL. Engineering the Keratinocyte Microenvironment: Harnessing Topography to Direct Cellular Function. [Doctoral Dissertation]. Worcester Polytechnic Institute; 2015. Available from: etd-011215-151605 ; https://digitalcommons.wpi.edu/etd-dissertations/23

Universitat de Valencia

20. Carceller Zazo, Elena. Analysis of the molecular mechanisms that mediate the therapeutic actions of glucocorticoids in skin .

Degree: 2017, Universitat de Valencia

URL: http://hdl.handle.net/10550/59278

► Los glucocorticoides (GCs) sintéticos han sido ampliamente utilizados para el tratamiento de las enfermedades autoinmunes e inflamatorias y ejercen sus acciones mediante la unión al… (more)

▼ Los glucocorticoides (GCs) sintéticos han sido ampliamente utilizados para el tratamiento de las enfermedades autoinmunes e inflamatorias y ejercen sus acciones mediante la unión al receptor de GCs (GR en inglés) (Ramamoorthy y Cidlowski, 2016). GR es un factor de transcripción (TF en inglés) que pertenece a la superfamilia de receptores nucleares que media importantes procesos fisiológicos (Sacta et al., 2016). Tras la unión del ligando, GR se transloca al núcleo y ejerce sus acciones mediante la unión a DNA o interaccionando con otros factores de transcripción. La regulación transcripcional directa por GR implica su unión a secuencias reguladoras de ADN específicas llamadas elementos de respuesta a GC o GREs. Durante mucho tiempo, se postuló que GR inducía sus efectos antiinflamatorios exclusivamente a través de la transrepresión mediante la inhibición de las vías inflamatorias conocidas, incluyendo NF-B, AP-1 y MAPKs (Weikum et al., 2017). Sin embargo, ahora se acepta que la inducción transcripcional de varias dianas clásicas que contienen GRE también es clave para las acciones anti-inflamatorias de GR (De Bosscher and Haegeman, 2009). El tratamiento continuo o altas dosis de GCs pueden producir efectos secundarios no deseados (atrofia de la piel), lo que puede tener un gran impacto en la población (Sacta et al., 2016). Por lo tanto, es importante comprender los mecanismos por los que GR regula la transcripción en la piel y su impacto en los efectos terapéuticos y adversos de los GCs. En la parte I de esta tesis se estudió la regulación de GC-induced leucine zipper (Gilz/Tsc22d3) y Zinc Finger Protein 36/Tristetraprolin (Zfp36/Ttp), dos dianas transcripcionales primarias de GR que contienen motivos de unión GRE, en queratinocitos epidérmicos. Éstas y otras dianas de GCs se han identificado previamente en el laboratorio mediante ensayos GR ChIP-seq en los que GRE, Krüppel-like factor (KLF), y AP-1 eran los motivos de unión más sobre-representados. Dada la relevancia de GR y KLF4 en la piel, hemos analizado las interacciones funcionales entre estos factores de transcripción y su impacto en la expresión de los genes Gilz/Tsc22d3 y Zfp36/Ttp. Los experimentos de pérdida de función de GR y KLF4 mostraron un requisito total de GR pero parcial de KLF4 para la completa inducción de genes en respuesta a dexametasona (Dex). En los queratinocitos terminalmente diferenciados inducidos por calcio, la expresión de la proteína GR y KLF4 aumentó coincidiendo con el aumento de Gilz/Tsc22d3 y Zfp36/Ttp. Sin embargo, las células deficientes en GR no lograron diferenciar o inducir completamente Gilz, Zfp36 y Klf4, correlacionando con el aumento de la expresión de Trp63, un conocido represor transcripcional de KLF4 que es específico del epitelio. La cooperación transcripcional identificada entre GR y KLF4 puede que determine la regulación específica del tipo celular y tiene implicaciones para el desarrollo de terapias para enfermedades de la piel. En la parte II de esta tesis, hemos investigado GILZ, que se ha demostrado… Advisors/Committee Members: Pérez Sánchez, Paloma (advisor).

Subjects/Keywords: gilz; glucocorticoid receptor; zfp36; klf4; keratinocyte; mouse; skin

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Carceller Zazo, E. (2017). Analysis of the molecular mechanisms that mediate the therapeutic actions of glucocorticoids in skin . (Doctoral Dissertation). Universitat de Valencia. Retrieved from http://hdl.handle.net/10550/59278

Chicago Manual of Style (16^th Edition):

Carceller Zazo, Elena. “Analysis of the molecular mechanisms that mediate the therapeutic actions of glucocorticoids in skin .” 2017. Doctoral Dissertation, Universitat de Valencia. Accessed January 25, 2021. http://hdl.handle.net/10550/59278.

MLA Handbook (7^th Edition):

Carceller Zazo, Elena. “Analysis of the molecular mechanisms that mediate the therapeutic actions of glucocorticoids in skin .” 2017. Web. 25 Jan 2021.

Vancouver:

Carceller Zazo E. Analysis of the molecular mechanisms that mediate the therapeutic actions of glucocorticoids in skin . [Internet] [Doctoral dissertation]. Universitat de Valencia; 2017. [cited 2021 Jan 25]. Available from: http://hdl.handle.net/10550/59278.

Council of Science Editors:

Carceller Zazo E. Analysis of the molecular mechanisms that mediate the therapeutic actions of glucocorticoids in skin . [Doctoral Dissertation]. Universitat de Valencia; 2017. Available from: http://hdl.handle.net/10550/59278

Universitat de Valencia

21. Sanchis Gandía, Ana. Estudio funcional del receptor de glucocorticoides en desarrollo y reparación epitelial .

Degree: 2013, Universitat de Valencia

URL: http://hdl.handle.net/10550/29048

► El receptor de glucocorticoides (GR) juega un papel crucial en la morfogénesis epidérmica durante el desarrollo embrionario, como se ha demostrado mediante el análisis de… (more)

▼ El receptor de glucocorticoides (GR) juega un papel crucial en la morfogénesis epidérmica durante el desarrollo embrionario, como se ha demostrado mediante el análisis de modelos de ratones genéticamente modificados con ganancia y pérdida de función de GR. La formación del párpado constituye un modelo útil para estudiar el desarrollo epitelial, ya que requiere de la regulación coordinada de la proliferación de queratinocitos, la apoptosis y la migración. Hemos analizado este proceso biológico en embriones GR-/ - durante la ontogenia. Nuestros datos demuestran que la deficiencia de GR en el cierre de los párpados da como resultado un proceso de cierre anómalo y retrasado, como se ilustra por el aumento de la proliferación de queratinocitos y la apoptosis, junto con una alteración de la diferenciación en las células epiteliales de los párpados GR-/ -. Estos defectos se deben, al menos en parte, a la falta de antagonismo entre la vía de señalización de GR y el factor de crecimiento epidérmico (EGFR), causando la activación sostenida de la vía de MAPK/AP-1 y la regulación al alza de la queratina K6 en la etapa embrionaria E18.5 . Además, se demuestra que GR regula la migración de células epiteliales in vitro al interferir con la señalización mediada por EGFR. En general, el antagonismo GR / EGFR aparece como un importante mecanismo que regula el desarrollo del epitelio ocular. La cicatrización cutánea es un proceso complejo de comienza después de una lesión, orientado a reparar el daño a los tejidos y restaurar la homeostasis de la piel. Hay tres fases en este proceso que requieran una interacción coordinada entre los diversos tipos celulares con una cinética precisa: la inflamación, la re-epitelización y remodelación tisular. Es bien sabido que el tratamiento con glucocorticoides (GC) produce un retraso en la cicatrización de heridas, que es uno de los efectos secundarios adversos más comunes asociados al uso terapéutico GC. Hemos evaluado la contribución específica del receptor GC (GR) en la cicatrización de heridas con ratones que sobre-expresan constitutiva GR WT o una forma mutante de GR defectivo en transactivación (transgénicos K5-GR y K5-GR-TR). Este enfoque nos permite comparar in vivo los mecanismos de acción GR, tanto dependientes de unión a DNA como independientes de unión a DNA. Las heridas K5-GR cicatrizan más lentamente que el WT según la evaluación de la cinética de cierre de la herida en días (d) 4 y 8 después de la lesión, que muestra una reducción del reclutamiento de granulocitos / macrófagos, así como la disminución de expresión de TNF-a e IL-6. Los niveles de mRNA de IL-1 B, KGF y TGF-B1 fueron reprimidos por GR, mientras que TGF-B3 fue reguladas al alza. La tasa de re-epitelización, determinada por la proliferación de queratinocitos y la migración, se redujo en las heridas K5-GR en relación con WT, junto con un deterioro de la formación de tejido de granulación. En contraste, los ratones K5-GR-TR mostraron retraso en la cicatrización en d4, pero re-establecen la herida de la piel en d8… Advisors/Committee Members: Pérez Sánchez, Paloma (advisor).

Subjects/Keywords: wound healing; keratinocyte; genetically modified mice; eye development skin; glucocorticoid receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sanchis Gandía, A. (2013). Estudio funcional del receptor de glucocorticoides en desarrollo y reparación epitelial . (Doctoral Dissertation). Universitat de Valencia. Retrieved from http://hdl.handle.net/10550/29048

Chicago Manual of Style (16^th Edition):

Sanchis Gandía, Ana. “Estudio funcional del receptor de glucocorticoides en desarrollo y reparación epitelial .” 2013. Doctoral Dissertation, Universitat de Valencia. Accessed January 25, 2021. http://hdl.handle.net/10550/29048.

MLA Handbook (7^th Edition):

Sanchis Gandía, Ana. “Estudio funcional del receptor de glucocorticoides en desarrollo y reparación epitelial .” 2013. Web. 25 Jan 2021.

Vancouver:

Sanchis Gandía A. Estudio funcional del receptor de glucocorticoides en desarrollo y reparación epitelial . [Internet] [Doctoral dissertation]. Universitat de Valencia; 2013. [cited 2021 Jan 25]. Available from: http://hdl.handle.net/10550/29048.

Council of Science Editors:

Sanchis Gandía A. Estudio funcional del receptor de glucocorticoides en desarrollo y reparación epitelial . [Doctoral Dissertation]. Universitat de Valencia; 2013. Available from: http://hdl.handle.net/10550/29048

Loyola University Chicago

22. Larm, Ashley Lynn. Characterizing the Mechanisms by Which Community Associated Methicillin-Resistant Staphylococcus Aureus Influences Keratinocyte Innate Immune Responses During Recurrent Infection.

Degree: MS, Biological Science, 2014, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_theses/2627

► Community associated–methicillin resistant Staphylococcus aureus (CA–MRSA) infection has become a major health concern. In human epidermal keratinocytes, S. aureus is mainly recognized through toll–like… (more)

Subjects/Keywords: Community-associated MRSA; Keratinocyte immune response; Immunology and Infectious Disease

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APA (6^th Edition):

Larm, A. L. (2014). Characterizing the Mechanisms by Which Community Associated Methicillin-Resistant Staphylococcus Aureus Influences Keratinocyte Innate Immune Responses During Recurrent Infection. (Thesis). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_theses/2627

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Larm, Ashley Lynn. “Characterizing the Mechanisms by Which Community Associated Methicillin-Resistant Staphylococcus Aureus Influences Keratinocyte Innate Immune Responses During Recurrent Infection.” 2014. Thesis, Loyola University Chicago. Accessed January 25, 2021. https://ecommons.luc.edu/luc_theses/2627.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Larm, Ashley Lynn. “Characterizing the Mechanisms by Which Community Associated Methicillin-Resistant Staphylococcus Aureus Influences Keratinocyte Innate Immune Responses During Recurrent Infection.” 2014. Web. 25 Jan 2021.

Vancouver:

Larm AL. Characterizing the Mechanisms by Which Community Associated Methicillin-Resistant Staphylococcus Aureus Influences Keratinocyte Innate Immune Responses During Recurrent Infection. [Internet] [Thesis]. Loyola University Chicago; 2014. [cited 2021 Jan 25]. Available from: https://ecommons.luc.edu/luc_theses/2627.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Larm AL. Characterizing the Mechanisms by Which Community Associated Methicillin-Resistant Staphylococcus Aureus Influences Keratinocyte Innate Immune Responses During Recurrent Infection. [Thesis]. Loyola University Chicago; 2014. Available from: https://ecommons.luc.edu/luc_theses/2627

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of British Columbia

23. Li, Min. KGF-1 and KGF receptor expression in human periodontal disease and in vitro microwounding-associated-ligand-independent KGFR activation.

Degree: PhD, Dental Science, 2007, University of British Columbia

URL: http://hdl.handle.net/2429/418

► Objectives: Periodontal disease is a chronic inflammation resulting in periodontal attachment loss. Keratinocyte Growth Factor-1 (KGF-1) is upregulated in chronic inflammation and specifically stimulates epithelial… (more)

▼ Objectives: Periodontal disease is a chronic inflammation resulting in periodontal attachment loss. Keratinocyte Growth Factor-1 (KGF-1) is upregulated in chronic inflammation and specifically stimulates epithelial cell proliferation by signaling through the epithelial-specific Keratinocyte Growth Factor Receptor (KGFR). First, we examined KGF-1 and KGFR expression and localization in human periodontal tissues. Second, we extended these studies by developing an in vitro mechanical wound model to mimic trauma to the periodontal pocket epithelium and examined ligand independent KGFR activation and cell migration. Methods: In our study of human gingival tissues, we used immunohistochemistry and laser capture microdissection with RT-PCR to analyze KGF-1 and KGFR expression and localization. To study ligand independent KGFR phosphorylation, KGFR internalization along the wound edge was imaged using immunohistochemical staining and KGFR phosphorylation confirmed using immunoprecipitation with western blotting. Wounding induced oxidative stress was detected using DCFH-DA (2',7'-dichlorofluorescin diacetate) and modulated by pretreatment with an antioxidant. Changes in migration were examined in the presence or absence of pathway specific inhibitors. Results: KGF-1 protein localized to areas of junctional and basal oral epithelial cells was significantly increased in periodontal pocket epithelium (p<0.01) and oral epithelium (p<0.05) of disease-associated tissues. KGFR localized to the junctional and the parabasal cells of oral epithelium, and was increased in disease-associated pocket epithelium (p<0.05). Laser capture microdissection with RT-PCR confirmedKGF-1 and KGFR were specifically expressed by connective tissue and epithelium, respectively. In our cell culture model, mechanical wounding induced ligand independent KGFR activation. ROS (Reactive Oxygen Species) generation along the wound edge was associated with KGFR activation and scavenging of ROS reduced KGFR phosphorylation. The c-Src family inhibitor, PP1, significantly inhibited KGFR phosphorylation. Functionally cell migration was reduced by PP1 (82.7%), SU5402(70%) and PD98059 (57%). Conclusions: KGF-1 and KGFR proteins are expressed in health but significantly induced in human diseased periodontal tissues. Microwounding associated generation of ROS mediates KGFR phosphorylation via c-Src kinase signaling and induced wound edge cell migration. Therefore, regulation of epithelial cell behavior associated with the onset and progression of periodontal disease may possibly be mediated by two related but distinct mechanisms. (1) Ligand-dependent activation of KGFR due to upregulation of KGF-1. (2) Ligand-independent activation of KGFR due to chronic microwounding.

Subjects/Keywords: periodontal disease; keratinocyte; KGFR; ligand

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APA (6^th Edition):

Li, M. (2007). KGF-1 and KGF receptor expression in human periodontal disease and in vitro microwounding-associated-ligand-independent KGFR activation. (Doctoral Dissertation). University of British Columbia. Retrieved from http://hdl.handle.net/2429/418

Chicago Manual of Style (16^th Edition):

Li, Min. “KGF-1 and KGF receptor expression in human periodontal disease and in vitro microwounding-associated-ligand-independent KGFR activation.” 2007. Doctoral Dissertation, University of British Columbia. Accessed January 25, 2021. http://hdl.handle.net/2429/418.

MLA Handbook (7^th Edition):

Li, Min. “KGF-1 and KGF receptor expression in human periodontal disease and in vitro microwounding-associated-ligand-independent KGFR activation.” 2007. Web. 25 Jan 2021.

Vancouver:

Li M. KGF-1 and KGF receptor expression in human periodontal disease and in vitro microwounding-associated-ligand-independent KGFR activation. [Internet] [Doctoral dissertation]. University of British Columbia; 2007. [cited 2021 Jan 25]. Available from: http://hdl.handle.net/2429/418.

Council of Science Editors:

Li M. KGF-1 and KGF receptor expression in human periodontal disease and in vitro microwounding-associated-ligand-independent KGFR activation. [Doctoral Dissertation]. University of British Columbia; 2007. Available from: http://hdl.handle.net/2429/418

24. Sturniolo, Michael Thomas. Tazarotene-Induced Gene 3: A Novel Regulator of Keratinocyte Differentiation.

Degree: PhD, Molecular Virology, 2005, Case Western Reserve University School of Graduate Studies

URL: http://rave.ohiolink.edu/etdc/view?acc_num=case1100296278

► Tazarotene-induced gene 3 (TIG3) is a novel regulatory protein expressed in the human epidermis. TIG3 expression in keratinocytes results in a decrease in both proliferation… (more)

Subjects/Keywords: Biology, Cell; TIG3; Transglutaminase; Keratinocyte

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APA (6^th Edition):

Sturniolo, M. T. (2005). Tazarotene-Induced Gene 3: A Novel Regulator of Keratinocyte Differentiation. (Doctoral Dissertation). Case Western Reserve University School of Graduate Studies. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=case1100296278

Chicago Manual of Style (16^th Edition):

Sturniolo, Michael Thomas. “Tazarotene-Induced Gene 3: A Novel Regulator of Keratinocyte Differentiation.” 2005. Doctoral Dissertation, Case Western Reserve University School of Graduate Studies. Accessed January 25, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1100296278.

MLA Handbook (7^th Edition):

Sturniolo, Michael Thomas. “Tazarotene-Induced Gene 3: A Novel Regulator of Keratinocyte Differentiation.” 2005. Web. 25 Jan 2021.

Vancouver:

Sturniolo MT. Tazarotene-Induced Gene 3: A Novel Regulator of Keratinocyte Differentiation. [Internet] [Doctoral dissertation]. Case Western Reserve University School of Graduate Studies; 2005. [cited 2021 Jan 25]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1100296278.

Council of Science Editors:

Sturniolo MT. Tazarotene-Induced Gene 3: A Novel Regulator of Keratinocyte Differentiation. [Doctoral Dissertation]. Case Western Reserve University School of Graduate Studies; 2005. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1100296278

Wright State University

25. Abbas, Asma A. HSV-1 INFECTION IN KERATINOCYTE CELL LINES TREATED WITH MITOTIC INHIBITORS.

Degree: MS, Microbiology and Immunology, 2011, Wright State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=wright1303839668

► The hypothesis for this research was: Herpes simplex virus type 1 (HSV-1) infection of murine keratinocyte cell lines (HEL-30 and PAM-212) treated with mitotic inhibitors… (more)

Subjects/Keywords: Immunology; HSV-1 infection; keratinocyte cell lines; mitotic inhibitors

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APA (6^th Edition):

Abbas, A. A. (2011). HSV-1 INFECTION IN KERATINOCYTE CELL LINES TREATED WITH MITOTIC INHIBITORS. (Masters Thesis). Wright State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=wright1303839668

Chicago Manual of Style (16^th Edition):

Abbas, Asma A. “HSV-1 INFECTION IN KERATINOCYTE CELL LINES TREATED WITH MITOTIC INHIBITORS.” 2011. Masters Thesis, Wright State University. Accessed January 25, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1303839668.

MLA Handbook (7^th Edition):

Abbas, Asma A. “HSV-1 INFECTION IN KERATINOCYTE CELL LINES TREATED WITH MITOTIC INHIBITORS.” 2011. Web. 25 Jan 2021.

Vancouver:

Abbas AA. HSV-1 INFECTION IN KERATINOCYTE CELL LINES TREATED WITH MITOTIC INHIBITORS. [Internet] [Masters thesis]. Wright State University; 2011. [cited 2021 Jan 25]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1303839668.

Council of Science Editors:

Abbas AA. HSV-1 INFECTION IN KERATINOCYTE CELL LINES TREATED WITH MITOTIC INHIBITORS. [Masters Thesis]. Wright State University; 2011. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=wright1303839668

The Ohio State University

26. Johnson, Kelly Elizabeth. Direct Effects of VEGF on Keratinocyte Function During Skin Carcinogenesis and Wound Healing.

Degree: PhD, Integrated Biomedical Science Graduate Program, 2013, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1376662806

► Epidermal keratinocytes, the predominant cell type in the epidermis, play a crucial role in two processes in the skin: skin carcinogenesis and cutaneous wound healing.… (more)

▼ Epidermal keratinocytes, the predominant cell type in the epidermis, play a crucial role in two processes in the skin: skin carcinogenesis and cutaneous wound healing. Non-melanoma skin cancer (NMSC) is the most prevalent type of cancer, with 3.5 million cases diagnosed each year in the US. These cancers, including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) are primarily caused by exposure to ultraviolet (UV) light from the sun. Wound healing is a key process in many aspects of medicine. In addition to injury and trauma, millions of surgeries are performed each year. Chronic wounds, which do not heal properly, can lead to hospitalizations, amputations, death and affect 6.5 million patients every year at an estimated cost of $12 billion dollars. Therefore, it is critical to understand how keratinocytes function in both of these processes.Angiogenesis, the growth and expansion of new blood vessels, occurs during both NMSC and wound healing. Vascular endothelial growth factor (VEGF) promotes angiogenesis by causing the proliferation, migration and survival of vascular endothelial cells. VEGF is produced by the skin in response to UV and promotes NMSC indirectly through the induction of angiogenesis. Additionally, wounds contain high levels of VEGF. VEGF receptor 1 (VEGFR-1) has now been identified on epidermal keratinocytes, suggesting that VEGF can affect keratinocytes directly. Therefore, we hypothesize that VEGF may influence wound healing and skin carcinogenesis by directly affecting keratinocytes via VEGFR-1. To test this, a unique conditional knockout mouse with VEGFR-1-deficient keratinocytes (cKO) was developed and was utilized in acute and chronic UV-induced skin carcinogenesis studies as well as wound healing studies. Immunohistochemical analysis of human and murine NMSC samples revealed that VEGFR-1 is highly expressed in skin tumors. Furthermore, in vitro studies indicated that keratinocyte VEGF and VEGFR-1 expression is regulated by UV light. To examine the direct effects of VEGF on keratinocytes in skin carcinogenesis, cKO and control mice were exposed to acute and long term UV radiation. Keratinocytes in the epidermis of cKO mice showed a significant increase in apoptosis 24 hours following a single UV exposure compared to controls, suggesting that VEGF may function as a survival factor in UV-irradiated keratinocytes. Additionally, macrophage recruitment to UV damaged skin was reduced in cKO mice. Long term UV-induced skin carcinogenesis studies are ongoing and suggest that cKO mice are resistant to UV-induced skin carcinogenesis compared to controls. To examine the direct role of VEGF on keratinocytes in wound repair, excisional wounds were inflicted on cKO and control mice. A significant delay in reepithelialization was observed in cKO mice compared to controls 5 days after wounding. These results suggest that VEGF can stimulate epidermal keratinocytes directly to promote reepithelialization. Similar to acute UV studies, a significant decrease in the number of macrophages was observed… Advisors/Committee Members: Wilgus, Traci (Advisor).

Subjects/Keywords: Biomedical Research; skin; keratinocyte; VEGF; skin cancer; wound healing

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Johnson, K. E. (2013). Direct Effects of VEGF on Keratinocyte Function During Skin Carcinogenesis and Wound Healing. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1376662806

Chicago Manual of Style (16^th Edition):

Johnson, Kelly Elizabeth. “Direct Effects of VEGF on Keratinocyte Function During Skin Carcinogenesis and Wound Healing.” 2013. Doctoral Dissertation, The Ohio State University. Accessed January 25, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376662806.

MLA Handbook (7^th Edition):

Johnson, Kelly Elizabeth. “Direct Effects of VEGF on Keratinocyte Function During Skin Carcinogenesis and Wound Healing.” 2013. Web. 25 Jan 2021.

Vancouver:

Johnson KE. Direct Effects of VEGF on Keratinocyte Function During Skin Carcinogenesis and Wound Healing. [Internet] [Doctoral dissertation]. The Ohio State University; 2013. [cited 2021 Jan 25]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1376662806.

Council of Science Editors:

Johnson KE. Direct Effects of VEGF on Keratinocyte Function During Skin Carcinogenesis and Wound Healing. [Doctoral Dissertation]. The Ohio State University; 2013. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1376662806

University of Cambridge

27. Saunders-Wood, Taylor. Investigating Early Lesion Formation Following Papillomavirus Infection Using a Mouse Model and Cell Culture.

Degree: PhD, 2020, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/307401

► Papillomaviruses (PV) are small non-enveloped double-stranded DNA tumour viruses, which are able to infect more than 80 different host species. They are a diverse group… (more)

▼ Papillomaviruses (PV) are small non-enveloped double-stranded DNA tumour viruses, which are able to infect more than 80 different host species. They are a diverse group with over 400 types discovered, of which almost half infect humans. Human papillomaviruses have been linked to a myriad of diseases, including multiple cancers, recurrent respiratory papillomatosis, and genital warts. The disease burden of HPV-related conditions is severe, and there is currently no treatment that can guarantee eradication of viral infection. All PV types characterised so far have a similar genomic structure, and contain the so called 'core ORFs' – E1, E2, L1 and L2 which are essential for viral genome replication and packaging into infectious virions. PV evolution and diversification appears to have been impacted by the availability of certain epithelial niches, with co-evolution and niche adaptation allowing PVs to develop a remarkable species and tissue specificity. Consequently, the function of the PV early proteins can vary between different PV species and types, but as a group they share important organisational similarities that reflect their common requirement to infect and persist in the epithelium following infection. This has allowed the use of animal models to gain insight into the basic virus/host interactions that are targeted by this group of viruses as a whole. The mechanisms by which HPV establishes a lesion, particularly in low-risk types, are not fully understood. However, the recently identified mouse model of PV infection is a useful biological tool to study this period of PV infection in vivo. This body of work aims to expand current knowledge of early events in the PV life cycle. To further understand the mechanisms of cell persistence during PV infection, immunodeficient mouse tail samples inoculated with MmuPV1 were examined to investigate early lesion formation. Five discrete stages of lesion formation were characterised in the immunodeficient animals. In parallel studies, microlesions were rarely observed in immunocompetent C57BL/6J mice, reaching stage three of lesion formation. In-depth tissue analysis suggested a modulation of basal cell density in infected epithelium, and a delay in normal differentiation commitment in E6/E7 expressing cells. Whole genome cell culture experiments were attempted in parallel with human high-risk types, which showed a post-confluent effect of high concentration EGF on cell growth and genome copy number in cells containing HPV16 genomes. A role for MmuPV1 E6 in growth of cell populations to significantly higher densities was shown through experimentation with cells exogenously expressing viral proteins. Differentiation was also delayed in the cells expressing MmuPV1 E6, demonstrating a recapitulation of events characterised in in vivo infections. Novel use of fluorescent cell lines in tandem with confocal microscopy allowed innovative analysis of a high-density monolayer cell culture model. These experiments revealed that MmuPV1 E6 expression resulted in preferential…

Subjects/Keywords: virology; papillomavirus; human papillomavirus; mouse model; homeostasis; cell biology; keratinocyte

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APA (6^th Edition):

Saunders-Wood, T. (2020). Investigating Early Lesion Formation Following Papillomavirus Infection Using a Mouse Model and Cell Culture. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/307401

Chicago Manual of Style (16^th Edition):

Saunders-Wood, Taylor. “Investigating Early Lesion Formation Following Papillomavirus Infection Using a Mouse Model and Cell Culture.” 2020. Doctoral Dissertation, University of Cambridge. Accessed January 25, 2021. https://www.repository.cam.ac.uk/handle/1810/307401.

MLA Handbook (7^th Edition):

Saunders-Wood, Taylor. “Investigating Early Lesion Formation Following Papillomavirus Infection Using a Mouse Model and Cell Culture.” 2020. Web. 25 Jan 2021.

Vancouver:

Saunders-Wood T. Investigating Early Lesion Formation Following Papillomavirus Infection Using a Mouse Model and Cell Culture. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Jan 25]. Available from: https://www.repository.cam.ac.uk/handle/1810/307401.

Council of Science Editors:

Saunders-Wood T. Investigating Early Lesion Formation Following Papillomavirus Infection Using a Mouse Model and Cell Culture. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/307401

Penn State University

28. Chapman, Sandra Elizabeth. ANALYZING THE REGULATION OF HPV REPLICATION AND TRANSCRIPTION IN ITS NATURAL HOST, THE KERATINOCYTE .

Degree: 2010, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/11273

► Each papillomavirus is species specific and replicates persistently in a specific type of cutaneous or mucosal epithelium. The keratinocytes of the basal layer of the… (more)

▼ Each papillomavirus is species specific and replicates persistently in a specific type of cutaneous or mucosal epithelium. The keratinocytes of the basal layer of the epithelium harbor a reservoir of replicating viral genomes. The processes of the HPV life cycle depend on elements in the viral genome that are regulated by host cell specific factors and therefore, ideally, analyses of viral transcription and replication should be carried out in primary keratinocytes. However, these studies are limited by the current cell culture and transfection methods. Improvements in the transfection and culture of keratinocytes will enable more sensitive, accurate and earlier analyses of viral replication and transcription. To test this we developed an optimized keratinocyte culture system using a Rho-Kinase (ROCK) inhibitor, Y-27632, that greatly improved the growth rate of primary keratinocytes and immortalized these cells. Further analysis revealed that the immortalized keratinocytes appeared to retain important characteristic of primary keratinocytes important for HPV research. Transient HPV replication analysis was enhanced in Y-27632-treated keratinocytes, presumably due to improved transfection efficiency and survival of transfected cells. Thus, improvements in primary cell culture and survival after transfection vastly improve the study of the establishment of HPV gene expression and replication. This allowed us to develop a complementation assay to study elements important for viral DNA replication. Using the complementation assay and the Y-27632 treated cells we were able to confirm the significance of the three E2 binding sites most proximal to the E6 promoter for transient replication. Finally, we designed immortalization assays using complete HPV genomes with targeted mutations to confirm that the information amassed from reporter assays holds up in more physiologically relevant systems. We were able to demonstrate that the TATA box, the Sp1 site, and the Ap1 site proximal to the E6 promoter, but not the distal Ap1 site, were dispensable for E6 and E7 expression. Collectively, these studies shed light on the significance of previously identified regulatory elements in the HPV life cycle as well as offer new strategies for future HPV life cycle studies. Advisors/Committee Members: Craig Matthew Meyers, Dissertation Advisor/Co-Advisor, Craig Matthew Meyers, Committee Chair/Co-Chair, Alison Mc Bride, Committee Chair/Co-Chair, Diane M Thiboutot, Committee Member, Jianming Hu, Committee Member, Neil David Christensen, Committee Member.

Subjects/Keywords: transcription; papillomaviruses; keratinocyte; immortalization; differentiation; replication

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APA (6^th Edition):

Chapman, S. E. (2010). ANALYZING THE REGULATION OF HPV REPLICATION AND TRANSCRIPTION IN ITS NATURAL HOST, THE KERATINOCYTE . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/11273

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Chapman, Sandra Elizabeth. “ANALYZING THE REGULATION OF HPV REPLICATION AND TRANSCRIPTION IN ITS NATURAL HOST, THE KERATINOCYTE .” 2010. Thesis, Penn State University. Accessed January 25, 2021. https://submit-etda.libraries.psu.edu/catalog/11273.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Chapman, Sandra Elizabeth. “ANALYZING THE REGULATION OF HPV REPLICATION AND TRANSCRIPTION IN ITS NATURAL HOST, THE KERATINOCYTE .” 2010. Web. 25 Jan 2021.

Vancouver:

Chapman SE. ANALYZING THE REGULATION OF HPV REPLICATION AND TRANSCRIPTION IN ITS NATURAL HOST, THE KERATINOCYTE . [Internet] [Thesis]. Penn State University; 2010. [cited 2021 Jan 25]. Available from: https://submit-etda.libraries.psu.edu/catalog/11273.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chapman SE. ANALYZING THE REGULATION OF HPV REPLICATION AND TRANSCRIPTION IN ITS NATURAL HOST, THE KERATINOCYTE . [Thesis]. Penn State University; 2010. Available from: https://submit-etda.libraries.psu.edu/catalog/11273

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

29. O'Neill, Adrian Thomas. A Microfluidic Platform for Human Epidermal Keratinocyte Cytotoxicity Assays.

Degree: PhD, Biomedical Engineering, 2009, North Carolina State University

URL: http://www.lib.ncsu.edu/resolver/1840.16/5477

► Linear dilution is a method to create linearly varying concentrations of a solution. Linear dilutions are commonly used in biological studies where the threshold concentration… (more)

▼ Linear dilution is a method to create linearly varying concentrations of a solution. Linear dilutions are commonly used in biological studies where the threshold concentration at which a physiological reaction occurs is unknown, whether it be a minimum effective or a maximum tolerable dosage. In this dissertation we present a summary of the approaches used for creating dilutions with microfluidics followed by a detailed methodology for constructing a proportional mixing linear dilution microfluidic device. The microfluidic device presented here is made with a rapid and inexpensive microfabrication method, soft lithography. The device is capable of generating nine linearly varying dilution values with an R-squared value exceeding 0.999 and the linearity of the dilutions is independent of the input flowrate, making it a very robust approach to creating linear dilutions. With the model presented the device can be expanded to an arbitrary number of dilutions with commensurate savings in reagent usage and time. Human epidermal keratinocytes (HEK) are skin cells of primary importance in maintaining the bodyÃ¢â‚¬â„¢s defensive barrier and are used in vitro to assess the irritation potential and toxicity of chemical compounds. Microfluidic systems hold promise for high throughput irritant and toxicity assays, but HEK growth kinetics have yet to be characterized within microscale culture chambers. This research demonstrates HEK patterning on microscale patches of Type I collagen within microfluidic channels and maintenance of these cells under constant medium perfusion for 72 h. HEK were shown to maintain 93.0% - 99.6% viability at 72 h under medium perfusion ranging from 0.025 Ã¢â‚¬â€œ 0.4 microliters per minute. HEK maintained this viability while ~100% confluentÃ¢â‚¬â€ a level not possible in 96 well plates. Microscale HEK cultures offer the ability to precisely examine the morphology, behavior and viability of individual cells which may open the door to new discoveries in toxicological screening methods and wound healing techniques. A microfabricated cell curtain is presented that facilitates cellular assays. The cell curtain is defined as a poly(dimethylsiloxane) (PDMS) wall that extends from the ceiling of a cell culture microchamber to within microns of the chamber floor. Curtain use is demonstrated by observing monolayer human epidermal keratinocyte (HEK) colonies for 48 hrs longer than possible with non-curtained microfluidic chambers. The curtains were further characterized by integrating them into a 96-chamber high-throughput microfluidic cell culture device. As proof of concept, this device was used to assay a range of ethanol dilutions spanning 0 Ã¢â‚¬â€œ 22% in cell culture medium. Cells exposed to 12% ethanol or less for 30 min would recover to 85% viability at 24 hr, while cells exposed to higher concentrations had viabilities below 10%. The data also showed that cells exposed to 6% ethanol or less grew in population size, 8% ethanol exposure stunted growth, and higher concentrations led to population loss.… Advisors/Committee Members: Henry Hsiao, Committee Member (advisor), Edward Grant, Committee Member (advisor), Nancy Monteiro-Riviere, Committee Member (advisor), Greg McCarty, Committee Member (advisor), Glenn Walker, Committee Chair (advisor).

Subjects/Keywords: keratinocyte; cytotoxicity; dilution; microfluidics; PDMS

…keratinocyte irritation studies. Exogenous noxes may also induce the release of IL-1α, IL-1β, IL-6… …differentiation factor and stimulates keratinocyte proliferation. IL-8 release is a good indicator of… …irradiated human keratinocyte cell line: potential role of nitric oxide. FASEB J. 13, 1817-1824… …keratinocyte-derived cytokines in chemical toxicity. Toxicol. Lett. 82-83, 471-476. Monteiro-Riviere… …Assessment of Nanotube Cytotoxicity using Human Keratinocyte Cells. J. Toxicol. Environ. Health…

10 more images…

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APA (6^th Edition):

O'Neill, A. T. (2009). A Microfluidic Platform for Human Epidermal Keratinocyte Cytotoxicity Assays. (Doctoral Dissertation). North Carolina State University. Retrieved from http://www.lib.ncsu.edu/resolver/1840.16/5477

Chicago Manual of Style (16^th Edition):

O'Neill, Adrian Thomas. “A Microfluidic Platform for Human Epidermal Keratinocyte Cytotoxicity Assays.” 2009. Doctoral Dissertation, North Carolina State University. Accessed January 25, 2021. http://www.lib.ncsu.edu/resolver/1840.16/5477.

MLA Handbook (7^th Edition):

O'Neill, Adrian Thomas. “A Microfluidic Platform for Human Epidermal Keratinocyte Cytotoxicity Assays.” 2009. Web. 25 Jan 2021.

Vancouver:

O'Neill AT. A Microfluidic Platform for Human Epidermal Keratinocyte Cytotoxicity Assays. [Internet] [Doctoral dissertation]. North Carolina State University; 2009. [cited 2021 Jan 25]. Available from: http://www.lib.ncsu.edu/resolver/1840.16/5477.

Council of Science Editors:

O'Neill AT. A Microfluidic Platform for Human Epidermal Keratinocyte Cytotoxicity Assays. [Doctoral Dissertation]. North Carolina State University; 2009. Available from: http://www.lib.ncsu.edu/resolver/1840.16/5477

30. Rabeony, Hanitriniaina. Étude de l'implication des cytokines dans l'inflammation cutanée et application à l'identification de cibles thérapeutiques pertinentes : Study of involvment of cytokines in skin inflammation and application to the identification of relevant therapeutic targets.

Degree: Docteur es, Biologie, médecine, santé, 2014, Poitiers

URL: http://www.theses.fr/2014POIT1404

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Un réseau de cytokine complexe a été décrit dans le psoriasis mettant en évidence le rôle central des cytokines proinflammatoires dans la physiopathologie de cette… (more)

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Un réseau de cytokine complexe a été décrit dans le psoriasis mettant en évidence le rôle central des cytokines proinflammatoires dans la physiopathologie de cette maladie. Notre tentative de modéliser l'inflammation cutanée a montré que la combinaison de l'IL-17A, IL-22, IL-1α, oncostatine M (OSM) et le TNFα, augmente de manière synergique l'expression de chimiokines et de peptides antimicrobiens, reflétant certaines caractéristiques du psoriasis. D'autres caractéristiques de cette maladie sont l'acanthose et le blocage de la différenciation des kératinocytes. Notre premier objectif était d'étudier le rôle respectif de ces cytokines sur la différenciation des kératinocytes en comparaison avec les lésions de patients psoriasiques. Toutes ces cytokines inhibent l'expression des marqueurs de différentiation des kératinocytes, parmi lesquelles l’IL-22 et l’OSM sont les plus puissantes et le mélange M5 présente des effets synergiques. Si l'IL-22 et l'OSM déclenchent plus spécifiquement l'hyperplasie épidermique et le blocage de la différenciation, l’IL-1α, IL-17A et le TNFα sont plutôt impliqués dans l'activation de l'immunité innée. Le rôle fonctionnel de chacune de ces cytokines in vivo a été étudié dans un modèle d'inflammation cutanée de type psoriasique induit par l'imiquimod (IMQ), un agoniste TLR7, en utilisant des souris déficientes en cytokines. L'absence de l'OSM ou de l'OSMRβ n'a pas modifié le développement des lésions inflammatoires induites par l’IMQ. Une hypothèse est que d'autres cytokines peuvent avoir des effets redondants avec l'OSM. L'absence de l'IL-22 chez la souris diminue partiellement les lésions cutanées induites par l'IMQ, démontrant que son retrait du réseau cytokinique rompt une partie des effets synergiques des cytokines in vivo comme présenté dans le modèle M5. L'absence de l'IL-1α ou de l'IL-1β ne modifie pas l'inflammation cutanée induite par l'IMQ, ce qui n'est pas surprenant au vu des activités redondantes de ces deux cytokines. La diminution partielle de l'inflammation en absence d'IL-1α ET d'IL-1β OU de la chaine réceptrice commune IL-1RI confirme ces observations. A long terme ces études devraient permettre de proposer des stratégies anti-cytokine ciblées et combinées pour tenter de rompre la synergie et diminuer ainsi toutes les composantes de la réponse inflammatoire cutanée.

A complex cytokine network has been described in psoriasis and highlighted a central role of proinflammatory cytokines produced by infiltrated immune cells. Our attempt to model skin inflammation showed that the combination of IL-17A, IL-22, IL-1α, OSM and TNFα (Mix M5) synergistically increases chemokines and antimicrobial-peptides expression, recapitulating some features of psoriasis. Other characteristics of psoriasis are acanthosis and down-regulation of keratinocyte differentiation markers. Our aim was to characterize the specific roles of these cytokines on keratinocyte differentiation, and to compare with psoriatic lesion features. All cytokines decrease keratinocytes differentiation markers…

Advisors/Committee Members: Morel, Franck (thesis director), Lecron, Jean-Claude (thesis director).

Subjects/Keywords: Psoriasis; Kératinocyte; Inflammation; Cytokine; Différenciation; Imiquimod; Psoriasis; Keratinocyte; Inflammation; Cytokine; Differentiation; Imiquimod; 616.526

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APA (6^th Edition):

Rabeony, H. (2014). Étude de l'implication des cytokines dans l'inflammation cutanée et application à l'identification de cibles thérapeutiques pertinentes : Study of involvment of cytokines in skin inflammation and application to the identification of relevant therapeutic targets. (Doctoral Dissertation). Poitiers. Retrieved from http://www.theses.fr/2014POIT1404

Chicago Manual of Style (16^th Edition):

Rabeony, Hanitriniaina. “Étude de l'implication des cytokines dans l'inflammation cutanée et application à l'identification de cibles thérapeutiques pertinentes : Study of involvment of cytokines in skin inflammation and application to the identification of relevant therapeutic targets.” 2014. Doctoral Dissertation, Poitiers. Accessed January 25, 2021. http://www.theses.fr/2014POIT1404.

MLA Handbook (7^th Edition):

Rabeony, Hanitriniaina. “Étude de l'implication des cytokines dans l'inflammation cutanée et application à l'identification de cibles thérapeutiques pertinentes : Study of involvment of cytokines in skin inflammation and application to the identification of relevant therapeutic targets.” 2014. Web. 25 Jan 2021.

Vancouver:

Rabeony H. Étude de l'implication des cytokines dans l'inflammation cutanée et application à l'identification de cibles thérapeutiques pertinentes : Study of involvment of cytokines in skin inflammation and application to the identification of relevant therapeutic targets. [Internet] [Doctoral dissertation]. Poitiers; 2014. [cited 2021 Jan 25]. Available from: http://www.theses.fr/2014POIT1404.

Council of Science Editors:

Rabeony H. Étude de l'implication des cytokines dans l'inflammation cutanée et application à l'identification de cibles thérapeutiques pertinentes : Study of involvment of cytokines in skin inflammation and application to the identification of relevant therapeutic targets. [Doctoral Dissertation]. Poitiers; 2014. Available from: http://www.theses.fr/2014POIT1404

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