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You searched for subject:(TRPV6). Showing records 1 – 3 of 3 total matches.

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Penn State University

1. McCarthy, Sarah Anne. A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases.

Degree: 2012, Penn State University

There are currently no effective therapeutic treatments to prevent prostate cancer (PCa) bone metastases. Identifying mechanisms that facilitate favorable PCa cell to bone interactions will aid in the development of therapies to prevent bone metastases. The objective of this study was to identify a role for calcium and Transient Receptor Potential Vanilloid 6 (TRPV6) ion channels in the metastatic potential and early colonization of osteoblastic PCa cells to murine bone. We proposed that transient increases in serum calcium, following parathyroid hormone (PTH) 1-34 administration, confers a metastatic advantage to PCa cells in circulation, signaled partially via TRPV6 ion channels. To identify the effect of transient elevations in calcium on osteoblastic PCa cell metastatic potential, we employed heterotypic cell adhesion, transwell migration, and invasion assays. Observations from cell adhesion assays suggested that osteoblastic PCa cells increased adhesion to human bone marrow endothelial (hbmE) cells pre-treated with extracellular calcium. Studies suggested that increased extracellular calcium enhanced E-Selectin, VCAM-1 and ICAM-1 cell surface abundance on hbmE cells and that these molecules were partially responsible for increased heterotypic cell adhesion. Increased extracellular calcium also enhanced migration of osteoblastic PCa cell lines, in vitro. To identify the requirement for TRPV6 expression in osteoblastic PCa cell metastatic potential, we reduced TRPV6 expression in osteoblastic PCa cell lines. PCa cells with reduced levels of TRPV6 expression demonstrated slower proliferation rates and an impaired ability to adhere to and invade hbmE cells. Lastly, to identify a role for TRPV6 expression in early PCa cell colonization of murine bone, SCID/Beige mice were administered PTH 1-34 or vehicle, intermittently, then inoculated with PCa cells engineered to express reduced levels of TRPV6. Eight weeks post PCa cell inoculation, PCa cells were identified in long bones of 100% of animals administered PTH 1-34, relative to 20% of animals treated with vehicle. In contrast, PCa cells were identified in only 20% of the long bones of animals administered PTH 1-34, and then inoculated with PCa cells with reduced TRPV6 expression. Our observations support our hypothesis and suggest that calcium and TRPV6 may have a role in facilitating favorable PCa cell to bone interactions. Advisors/Committee Members: Ronald R Gomes Jr, Dissertation Advisor/Co-Advisor, Henry Joseph Donahue, Committee Member, Patricia Mc Laughlin, Committee Member, Andrea Manni, Committee Member, Andrea Marie Mastro, Committee Member.

Subjects/Keywords: Prostate cancer; TRPV6; parathyroid hormone; osteoblastic; calcium; bone metastases; invasion; adhesion

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

APA (6th Edition):

McCarthy, S. A. (2012). A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/13790

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

Chicago Manual of Style (16th Edition):

McCarthy, Sarah Anne. “A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases.” 2012. Thesis, Penn State University. Accessed March 03, 2021. https://submit-etda.libraries.psu.edu/catalog/13790.

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

MLA Handbook (7th Edition):

McCarthy, Sarah Anne. “A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases.” 2012. Web. 03 Mar 2021.

Vancouver:

McCarthy SA. A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases. [Internet] [Thesis]. Penn State University; 2012. [cited 2021 Mar 03]. Available from: https://submit-etda.libraries.psu.edu/catalog/13790.

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

Council of Science Editors:

McCarthy SA. A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases. [Thesis]. Penn State University; 2012. Available from: https://submit-etda.libraries.psu.edu/catalog/13790

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


University of Zurich

2. Sprekeler, Nele. TRPV6 and Calbindin-D9k-expression and localisation in the bovine uterus and placenta during pregnancy.

Degree: 2012, University of Zurich

Transient receptor potential channel type 6 (TRPV6) and Calbindin-D9k (CaBP-9k) are involved in the active calcium (Ca2+) transport mechanism in many tissues including placenta and uterus, suggesting a role in the establishment and maintenance of pregnancy. Moreover, TRPV6 and CaBP-9k seem to support the materno-fetal Ca2+ transport that is crucial for fetal Ca2+ homeostasis, bone growth and development. However, it is unknown if these proteins are also involved in the aetiology of pathologies associated with parturition in cows, such as retained fetal membranes (RFM). The aim of the current study was to create an expression profile of uterine and placentomal TRPV6 and CaBP-9k mRNAs and proteins during pregnancy and postpartum in cows that discharged the fetal membranes in comparison to cows that retained them. The results of the present study demonstrate a dynamic expression of TRPV6 and CaBP-9k during pregnancy in the bovine uterine endometrium and placentomes, suggesting a functional role for these proteins in Ca2+ metabolism during pregnancy. The temporal and spatial expression patterns indicate that TRPV6 and CaBP-9k may be involved in materno-fetal Ca2+ transport, mainly through an interplacentomal transport, and that both proteins may participate in physiological processes that are crucial for fetal and placental development. However, neither TRPV6 nor CaBP-9k seem to be causative in the retention of fetal membranes. Transient receptor potential channel type 6 (TRPV6) und Calbindin-D9k (CaBP-9k) sind wichtige Elemente des aktiven Calcium (Ca2+) Transport in vielen Geweben und scheinen an der Etablierung und Aufrechterhaltung der Trächtigkeit beteiligt zu sein. Im Uterus sind TRPV6 und CaBP-9k als wichtige Faktoren für die myometriale Kontraktilität und Sekretion von Matrixkomponenten beschrieben. In der Plazenta scheinen beide Proteine am materno-fetalen Ca2+ Transport beteiligt zu sein. Ob TRPV6 und CaBP-9k ein Rolle in der Entstehung von Geburtspathologien spielen ist unbekannt. Das Ziel dieser Studie ist ein Expressionsprofil von uterinem und plazentärem TRPV6 und CaBP-9k Protein und mRNA während der Trächtigkeit des Rindes zu erstellen sowie die plazentäre Expression von Tieren mit Nachgeburtsverhaltung (NGV) der von Tieren mit physiologischer Nachgeburtsablösung gegenüberzustellen. Die Ergebnisse dieser Studie demonstrieren eine zeitlich dynamische Expression von TRPV6 und CaBP-9k in Uterus, Plazenta und fetalen Membranen und lassen einen Einfluss beider Proteine auf den Verlauf und Erhalt der Trächtigkeit des Rindes vermuten. Die Lokalisation sowie das zeitliche Expressionsmuster deuten auf eine Rolle beider Proteine am interplazentären materno-fetalen Ca2+-Transport hin. Zudem scheinen beide Proteine einen Einfluss auf die fetale und plazentäre Entwicklung zu haben. Dennoch scheinen weder TRPV6 noch CaBP-9k eine Rolle bei der Entstehung von NGV zu spielen.

Subjects/Keywords: Institute of Veterinary Anatomy; UZH Dissertations; 570 Life sciences; biology; TRPV6, Calbindin-D9k, cow, placenta, uterus, pregnancy

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

APA (6th Edition):

Sprekeler, N. (2012). TRPV6 and Calbindin-D9k-expression and localisation in the bovine uterus and placenta during pregnancy. (Thesis). University of Zurich. Retrieved from https://www.zora.uzh.ch/id/eprint/73505/1/Nele_Sprekeler.pdf

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

Chicago Manual of Style (16th Edition):

Sprekeler, Nele. “TRPV6 and Calbindin-D9k-expression and localisation in the bovine uterus and placenta during pregnancy.” 2012. Thesis, University of Zurich. Accessed March 03, 2021. https://www.zora.uzh.ch/id/eprint/73505/1/Nele_Sprekeler.pdf.

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

MLA Handbook (7th Edition):

Sprekeler, Nele. “TRPV6 and Calbindin-D9k-expression and localisation in the bovine uterus and placenta during pregnancy.” 2012. Web. 03 Mar 2021.

Vancouver:

Sprekeler N. TRPV6 and Calbindin-D9k-expression and localisation in the bovine uterus and placenta during pregnancy. [Internet] [Thesis]. University of Zurich; 2012. [cited 2021 Mar 03]. Available from: https://www.zora.uzh.ch/id/eprint/73505/1/Nele_Sprekeler.pdf.

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

Council of Science Editors:

Sprekeler N. TRPV6 and Calbindin-D9k-expression and localisation in the bovine uterus and placenta during pregnancy. [Thesis]. University of Zurich; 2012. Available from: https://www.zora.uzh.ch/id/eprint/73505/1/Nele_Sprekeler.pdf

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

3. Vachel, Laura. Étude de l'influx calcique des cellules épithéliales bronchiques mucoviscidosiques : implication des canaux TRP : Ca2+ influx in human bronchial epithelial cells : implication of TRP channels.

Degree: Docteur es, Aspects moléculaire et cellulaire de la biologie, 2014, Poitiers

Les canaux TRP (Transient Receptor Potential) sont des acteurs clés de l'homéostasie calcique. Plusieurs de ces canaux interviennent dans l'influx calcique des cellules épithéliales bronchiques, notamment TRPC6, qui est impliqué dans un couplage fonctionnel avec le canal Cystic Fibrosis Transmembrane conductance Regulator (CFTR). Les mutations du CFTR (F508del et G551D) sont à l'origine de la mucoviscidose (Cystic Fibrosis (CF)), qui aboutit à l'augmentation de l'influx calcique dans les cellules CF. L'objectif de ce travail a été d'étudier l'implication des canaux TRP dans la dérégulation de l'influx calcique des cellules épithéliales bronchiques CF. Nous avons mis en évidence que CFTR régulait négativement l'activité de TRPC6, tandis que l'influx calcique via TRPC6 permettait de potentialiser l'activité du canal muté CFTR-G551D, activé au préalable par le VX-770. Nous proposons donc une nouvelle stratégie thérapeutique, combinant un potentiateur de CFTR et un activateur spécifique de TRPC6. Nous nous sommes ensuite intéressés au rôle des canaux TRPV, en particulier TRPV5 et TRPV6, dans l'influx calcique des cellules épithéliales bronchiques. Nous avons observé que l'influx Ca2+ constitutif, attribuable à ces deux canaux, était doublé dans les cellules CF, dû à une augmentation de l'activité de TRPV6. En effet, l'expression de la PLC-δ1, une enzyme régulant négativement TRPV6, est dramatiquement réduite dans les cellules CF. La correction de l'adressage du F508del-CFTR a permis de normaliser l'activité de TRPV6 sans restaurer l'expression de la PLC-δ1 dans les cellules CF, suggérant un contrôle plus complexe de TRPV6 dans les cellules épithéliales bronchiques.

TRP (Transient Receptor Potential) channels are keys actors of Ca2+ homeostasis. Several of these channels are involved in the Ca2+ influx of bronchial epithelial cells, including TRPC6 which is implicated in a functional coupling with the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) channel. CFTR mutation leads Cystic Fibrosis (CF) disease and causes abnormal Ca2+ homeostasis trought an increased of Ca2+ influx in CF bronchial epithelial cells. Our objective is to investigate the implication of TRP channels in abnormal Ca2+ influx of CF bronchial epithelial cells.We showed that CFTR down regulates TRPC6 activity whereas Ca2+ influx through TRPC6 potentiates G551D-CFTR, activated by VX-770. We propose a new therapeutic strategy that combines a CFTR potentiator and a specific activator of TRPC6. Then, we focused on the role of TRPV channels, particularly TRPV5 and TRPV6, in Ca2+ influx of bronchial epithelial cells. We observed that constitutive Ca2+ influx, related to TRPV5/TRPV6 activity, was twice higher in CF cells due to the increase of TRPV6 activity. The expression of PLC-δ1, an enzyme that negatively regulates TRPV6 activity, is dramatically decreased in CF cells. The correction of F508del-CFTR trafficking allows TRPV6 activity normalization but do not restore PLC-δ1 expression level in CF cells, suggesting a more complex control of…

Advisors/Committee Members: Vandebrouck, Clarisse (thesis director).

Subjects/Keywords: Influx calcique; Cellules épithéliales bronchiques humaines; Mucoviscidose; Trpv6; Trpc6; PLC-Δ1; Cftr-G551d; CFTR-F508del; Calcium influx; Human bronchial epithelial cells; Cf; Trpv6; Trpc6; PLC-Δ1; Cftr-G551d; CFTR-F508del; 571.6

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

APA (6th Edition):

Vachel, L. (2014). Étude de l'influx calcique des cellules épithéliales bronchiques mucoviscidosiques : implication des canaux TRP : Ca2+ influx in human bronchial epithelial cells : implication of TRP channels. (Doctoral Dissertation). Poitiers. Retrieved from http://www.theses.fr/2014POIT2303

Chicago Manual of Style (16th Edition):

Vachel, Laura. “Étude de l'influx calcique des cellules épithéliales bronchiques mucoviscidosiques : implication des canaux TRP : Ca2+ influx in human bronchial epithelial cells : implication of TRP channels.” 2014. Doctoral Dissertation, Poitiers. Accessed March 03, 2021. http://www.theses.fr/2014POIT2303.

MLA Handbook (7th Edition):

Vachel, Laura. “Étude de l'influx calcique des cellules épithéliales bronchiques mucoviscidosiques : implication des canaux TRP : Ca2+ influx in human bronchial epithelial cells : implication of TRP channels.” 2014. Web. 03 Mar 2021.

Vancouver:

Vachel L. Étude de l'influx calcique des cellules épithéliales bronchiques mucoviscidosiques : implication des canaux TRP : Ca2+ influx in human bronchial epithelial cells : implication of TRP channels. [Internet] [Doctoral dissertation]. Poitiers; 2014. [cited 2021 Mar 03]. Available from: http://www.theses.fr/2014POIT2303.

Council of Science Editors:

Vachel L. Étude de l'influx calcique des cellules épithéliales bronchiques mucoviscidosiques : implication des canaux TRP : Ca2+ influx in human bronchial epithelial cells : implication of TRP channels. [Doctoral Dissertation]. Poitiers; 2014. Available from: http://www.theses.fr/2014POIT2303

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