subject:(branching morphogenesis)

University of California – Berkeley

1. Venugopalan, Gautham. External forces direct morphogenesis and tumorigenesis of the mammary gland.

Degree: Bioengineering, 2012, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/9wj5b96s

► Breast epithelia exist in a constant state of interaction with their surrounding environment. Morphogenesis is the developmental process by which breast cells grow into their… (more)

▼ Breast epithelia exist in a constant state of interaction with their surrounding environment. Morphogenesis is the developmental process by which breast cells grow into their surrounding matrix and form the ducts and milk-producing lobules. When morphogenesis breaks down, breast cancer occurs. Traditionally, biologists think of cancer through the framework of genetic mutations. Significant work in the past few decades demonstrated that the mechanical environment plays a critical role in determining growth and malignancy of breast cancers independent of genetic mutations. For example, increasing the stiffness of the extracellular matrix drives phenotypic malignancy through cell-generated contraction. However, the role of forces felt by the tissue due to external causes remains unclear. This dissertation describes experiments that reveal a critical role for external forces in branching morphogenesis and tumorigenesis. The experiments make use of a simple method to apply external compression to mammary epithelial cells embedded in biologically relevant gels. In branching, compression mechanically aligned collagen fibers and directed multicellular branch growth along these fibers. Fiber alignment sensing required fascin activity, but did not require RhoA-mediated contraction. Contraction served a separate purpose of generating fiber alignment in collagen networks. These findings suggest that migrating cells sense fiber alignment through fascin-mediated filopodia formation rather than through RhoA-mediated contraction.In tumorigenesis, compression encouraged malignant cells to form normal-looking acini, a process called `phenotypic reversion.' A transient compressive force at the one-cell state was sufficient to induce reversion without genetic manipulations or pharmacological treatments. Time-lapse microscopy of the malignant cells revealed that compression restored coherent rotation of malignant cell doublets, a behavior associated with the formation of a phenotypically normal structure. Blocking E-Cadherin eliminated compression sensitivity, indicating that cell-cell communication was required for force-induced reversion. As external forces altered the structure of a growing multicellular colony, changes in multicellular structure could affect epithelial mechanics. The mechanical properties of multicellular epithelial structures were measured using an atomic force microscope. Hollow lumen structures were softer than filled lumen structure. The increased stiffness associated with lumen filling could contribute to malignancy during cancer progression.Taken together, this work demonstrates the importance of external forces during morphogenesis and tumorigenesis of the mammary gland. External compression can direct multicellular migration and encourage malignant cells to re-enter the `normal' morphogenetic program. Cell-cell communication plays an important role in multicellular mechanosensing, contributing to both morphogenesis and mechanosensing in mammary epithelial structures. Further studies of multicellular…

Subjects/Keywords: Biomedical engineering; Biomechanics; Biophysics; acinar morphogenesis; applied forces; branching morphogenesis; breast cancer; cell mechanics; mechanosensing

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APA (6^th Edition):

Venugopalan, G. (2012). External forces direct morphogenesis and tumorigenesis of the mammary gland. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/9wj5b96s

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):

Venugopalan, Gautham. “External forces direct morphogenesis and tumorigenesis of the mammary gland.” 2012. Thesis, University of California – Berkeley. Accessed February 27, 2021. http://www.escholarship.org/uc/item/9wj5b96s.

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

MLA Handbook (7^th Edition):

Venugopalan, Gautham. “External forces direct morphogenesis and tumorigenesis of the mammary gland.” 2012. Web. 27 Feb 2021.

Vancouver:

Venugopalan G. External forces direct morphogenesis and tumorigenesis of the mammary gland. [Internet] [Thesis]. University of California – Berkeley; 2012. [cited 2021 Feb 27]. Available from: http://www.escholarship.org/uc/item/9wj5b96s.

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

Council of Science Editors:

Venugopalan G. External forces direct morphogenesis and tumorigenesis of the mammary gland. [Thesis]. University of California – Berkeley; 2012. Available from: http://www.escholarship.org/uc/item/9wj5b96s

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

University of California – Berkeley

2. Brownfield, Douglas Glenn. Characterization of the Interface between the Mouse Mammary Epithelium and its Microenvironment during Morphogenesis.

Degree: Bioengineering, 2011, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/2pf0d08b

► In characterizing the interface between the mammary epithelium and the microenvironment, it is necessary to first study specific components individually before interpreting the results in… (more)

▼ In characterizing the interface between the mammary epithelium and the microenvironment, it is necessary to first study specific components individually before interpreting the results in a larger context. With this in mind, the cell-cell component of the interface was first studied with respect to self-organization. Since initial experiments showed significant variance in size and morphology, a unique methodology was employed combining a micropatterning approach that confined cells to a cylindrical geometry with an algorithm to quantify changes of cellular distribution over time in order to measure the ability of different cell types to self-organize relative to each other. Using normal human mammary epithelial cells enriched into pools of the two principal lineages, luminal and myoepithelial cells, experiments demonstrated that bilayered organization in mammary epithelium was driven mainly by lineage-specific differential E-cadherin expression, but that P-cadherin contributed specifically to organization of the myoepithelial layer. Disruption of the actomyosin network or of adherens junction proteins resulted in either prevention of bilayer formation or loss of preformed bilayers, consistent with continual sampling of the local microenvironment by cadherins. Together these data show that self-organization is an innate and reversible property of communities of normal adult human mammary epithelial cells.Next, the cell-extracellular matrix (ECM) component was considered, focusing on the role of extracellular stiffness in both functional differentiation as well as branching morphogenesis. Since functional differentiation of the mammary epithelium involves the production of milk proteins such as caseins, a fluorescent reporter construct with the mouse beta-casein promoter was used as a metric for functional differentiation. This system was used for studies in which extracellular stiffness was tightly controlled and cellular stiffness measured and demonstrated a strong association between extra- and intracellular elasticity as well as functional differentiation in mammary epithelial cells (MECs). A benchmark for biomimetic intracellular elasticity was empirically determined via atomic force microscopy (AFM) measurements on normal mammary epithelium and used in subsequent experiments as a marker for the range of normal intracellular elasticity. The results established that maintenance of beta-casein expression required both laminin signaling and a `soft' extracellular matrix, as is the case in normal tissues in vivo, and biomimetic intracellular elasticity, as is the case in primary mammary epithelial organoids. Conversely, two hallmarks of breast cancer development, stiffening of the extracellular matrix and loss of laminin signaling, led to the loss of beta-casein expression and non-biomimetic intracellular elasticity. Extracellular stiffness was further plummeted with respect to branching morphogenesis by utilizing a three-dimensional culture model composed of type collagen-I. AFM was used to measure local…

Subjects/Keywords: Developmental biology; Cellular biology; Biomechanics; branching morphogenesis; ECM; mammary gland

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

APA (6^th Edition):

Brownfield, D. G. (2011). Characterization of the Interface between the Mouse Mammary Epithelium and its Microenvironment during Morphogenesis. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/2pf0d08b

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):

Brownfield, Douglas Glenn. “Characterization of the Interface between the Mouse Mammary Epithelium and its Microenvironment during Morphogenesis.” 2011. Thesis, University of California – Berkeley. Accessed February 27, 2021. http://www.escholarship.org/uc/item/2pf0d08b.

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

MLA Handbook (7^th Edition):

Brownfield, Douglas Glenn. “Characterization of the Interface between the Mouse Mammary Epithelium and its Microenvironment during Morphogenesis.” 2011. Web. 27 Feb 2021.

Vancouver:

Brownfield DG. Characterization of the Interface between the Mouse Mammary Epithelium and its Microenvironment during Morphogenesis. [Internet] [Thesis]. University of California – Berkeley; 2011. [cited 2021 Feb 27]. Available from: http://www.escholarship.org/uc/item/2pf0d08b.

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

Council of Science Editors:

Brownfield DG. Characterization of the Interface between the Mouse Mammary Epithelium and its Microenvironment during Morphogenesis. [Thesis]. University of California – Berkeley; 2011. Available from: http://www.escholarship.org/uc/item/2pf0d08b

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

Vanderbilt University

3. Vaught, David Bryan. EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis.

Degree: PhD, Cancer Biology, 2011, Vanderbilt University

URL: http://hdl.handle.net/1803/11610

► Eph receptor tyrosine kinases are membrane bound receptors often expressed by normal epithelial cells but are frequently overexpressed in many human cancers. Of the many… (more)

▼ Eph receptor tyrosine kinases are membrane bound receptors often expressed by normal epithelial cells but are frequently overexpressed in many human cancers. Of the many Eph receptors, EphA2 is present at low levels in normal mammary tissue but highly expressed in breast cancer and correlative with a poor patient prognosis. The focus of this thesis is to understand the endogenous role of EphA2 in mammary gland development and how overexpression can contribute to the poor prognosis through metastasis often seen with breast cancers overexpressing EphA2. Using EphA2-deficient animals, this thesis work demonstrates for the first time that EphA2 receptor function is required for mammary epithelial growth and branching morphogenesis. Loss of EphA2 decreased penetration of mammary epithelium into fat pad, reduced epithelial proliferation, and inhibited epithelial branching. These defects appear to be intrinsic to loss of EphA2 in epithelium, as transplantation of EphA2-deficient mammary tissue into wild-type recipient stroma recapitulated these defects. In addition, HGF-induced mammary epithelial branching morphogenesis was significantly reduced in EphA2-deficient cells relative to wild-type cells, which correlated with elevated basal RhoA activity. These results suggest that EphA2 receptor acts as a positive regulator in mammary gland development, functioning downstream of HGF to regulate branching through inhibition of RhoA. Breast cancer metastasis to bone is a major cause of morbidity and mortality in patients. Analysis of human breast-to-bone metastasis samples revealed EphA2 positive staining on tumor cells in close proximity to osteoclast at the tumor-bone interface. To define the role of EphA2 in tumor cell-host bone cell interactions, mouse tibias were injected with osteolytic breast tumor cells lacking EphA2 activity. Our data showed that inhibition of EphA2 activity significantly decreased tumor-induced osteolysis compared to controls. Further in vitro analysis revealed that blocking EphA2 function resulted in defective precursor maturation into functional osteoclasts. A human antibody targeted against EphA2 decreased breast tumor induced osteolysis in vivo. Our studies indicate the selective inhibition of EphA2 at the tumor-bone interface may be a benefit for the treatment of breast-to-bone metastases Advisors/Committee Members: Pampee Young (committee member), Charles Lin (committee member), Jin Chen (committee member), Lynn Matrisian (Committee Chair).

Subjects/Keywords: Branching Morphogenesis; Mammary Gland; Bone Metastasis; Breast Cancer; EphA2; IL-6

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

APA (6^th Edition):

Vaught, D. B. (2011). EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11610

Chicago Manual of Style (16^th Edition):

Vaught, David Bryan. “EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed February 27, 2021. http://hdl.handle.net/1803/11610.

MLA Handbook (7^th Edition):

Vaught, David Bryan. “EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis.” 2011. Web. 27 Feb 2021.

Vancouver:

Vaught DB. EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1803/11610.

Council of Science Editors:

Vaught DB. EphA2 receptor tyrosine kinase in mammary gland development and breast cancer induced osteolysis. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/11610

Vanderbilt University

4. Carver, Billy Joe. NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung.

Degree: PhD, Cell and Developmental Biology, 2013, Vanderbilt University

URL: http://hdl.handle.net/1803/13944

► Arrested lung development in preterm infants leads to bronchopulmonary dysplasia (BPD). Inflammation and NF-κB activation in the fetal lung inhibit airway morphogenesis and contribute to… (more)

Subjects/Keywords: inflammation; developmental biology; branching morphogenesis; NF-kappaB; mesenchymal cells; lung development

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

APA (6^th Edition):

Carver, B. J. (2013). NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13944

Chicago Manual of Style (16^th Edition):

Carver, Billy Joe. “NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed February 27, 2021. http://hdl.handle.net/1803/13944.

MLA Handbook (7^th Edition):

Carver, Billy Joe. “NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung.” 2013. Web. 27 Feb 2021.

Vancouver:

Carver BJ. NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1803/13944.

Council of Science Editors:

Carver BJ. NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/13944

University of Gothenburg / Göteborgs Universitet

5. Shawn, Liang. Growth regulation in thyroid development.

Degree: 2018, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/56262

► The fundamental aspects of developmental mechanisms that regulate embryonic and postnatal thyroid growth gaining the final size of the gland are still largely undetermined. In… (more)

▼ The fundamental aspects of developmental mechanisms that regulate embryonic and postnatal thyroid growth gaining the final size of the gland are still largely undetermined. In embryonic development, various organs and glands are composed of branched structures, designed to maximize efficiency and function. Branching morphogenesis is the developmental process that gives rise to these multicellular tubular networks. This growth process, which involves a range of paracrine and cell-autonomous factors including Fgf10 and Sox9, are utilized by the lung and numerous exocrine glands. In thyroid, an endocrine gland, postnatal growth involving thyroid stimulating hormone (TSH) from the pituitary differs to embryonic growth, which is TSH independent and thus rely on local factors of yet unknown identity. This thesis investigates thyroid growth regulation by Fgf10, Sox9, Shh and mutant Braf in normal (wildtype) and genetically modified mice engineered to constitutively or conditionally delete or express the targeted genes of interest. In paper I, we show that branching morphogenesis is a key process in glandular development of the embryonic thyroid. Sox9, Fgfr2b and Ki-67 are co-expressed at distal tips of branching epithelial buds. Mesenchymal Fgf10 is crucial for embryonic thyroid growth. The Fgf10-/- mutant thyroid has a normal anatomical shape and uninterrupted functional differentiation but is severely hypoplastic due to defective branching. These findings uncover a novel mechanism of thyroid development in which branching growth generated by reciprocal mesenchymal-epithelial interactions determines final organ size. Paper II investigates postnatal thyroid growth regulation. This identified growth retardation comprising reduced numbers of Ki-67+ proliferating cells in the thyroid of Fgf10+/- mutant mice. Thyroid growth is rescued postnatally in Fgf10+/-;Shh+/- double mutant animals, suggesting Shh regulation over Fgf10 signalling. This demonstrates for the first time gene dosage dependent regulation of postnatal thyroid growth accomplished through reciprocal interactions between Fgf10 and Shh signalling pathways. In Paper III, we examine effects of conditionally expressed Brafv600e oncoprotein in Nkx2-1+ progenitors on growth and differentiation of the embryonic thyroid. Constitutive activation of MAPK pathway by mutant Braf in thyroid progenitors lead to a global growth response and a 4-fold increase in thyroid size at birth, however without disturbing the natural morphogenesis to a bilobed gland or the differentiation into functional follicular cells. Thyroid specific gene analysis confirmed expression of Tg, Nis, Tpo, Tshr and Pax8, suggesting capability of iodination and thyroid hormone production in mutant embryonic cells. These results indicate that mechanisms of de novo thyroid differentiation in mouse embryos resist dedifferentiation as regularly observed in MAPK-activated adult thyroid cells. A potential clinical importance of this novel finding relies on the fact that thyroid tumour cells carrying…

Subjects/Keywords: Thyroid; growth regulation; branching morphogenesis; Fgf10; Sox9; Shh; Brafv600e

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

APA (6^th Edition):

Shawn, L. (2018). Growth regulation in thyroid development. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/56262

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):

Shawn, Liang. “Growth regulation in thyroid development.” 2018. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed February 27, 2021. http://hdl.handle.net/2077/56262.

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

MLA Handbook (7^th Edition):

Shawn, Liang. “Growth regulation in thyroid development.” 2018. Web. 27 Feb 2021.

Vancouver:

Shawn L. Growth regulation in thyroid development. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2018. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2077/56262.

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

Council of Science Editors:

Shawn L. Growth regulation in thyroid development. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2018. Available from: http://hdl.handle.net/2077/56262

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

Rice University

6. Martinez, Mariane. Role of cell-extracellular matrix interactions on tissue morphology, cell phenotype and organization in a salivary gland regeneration model.

Degree: PhD, Natural Sciences, 2019, Rice University

URL: http://hdl.handle.net/1911/105941

► Head and neck cancer affects over 64,000 Americans every year. Most of these patients receive radiation therapy as part of their standard treatment, which leads… (more)

▼ Head and neck cancer affects over 64,000 Americans every year. Most of these patients receive radiation therapy as part of their standard treatment, which leads to irradiation-induced xerostomia (dry mouth). Xerostomia drastically impairs these patients’ quality of life. Our lab proposes to develop a functional gland, suitable for re-implantation, from salivary-derived human stem/progenitor cells (hS/PCs) isolated from the patient before radiation therapy. Biocompatible hyaluronic acid (HA)-based hydrogels, functionalized with extracellular matrix (ECM)-derived peptides and seeded with hS/PCs and other support cells, will be used as a scaffold for bioengineering an autologous salivary gland replacement. The first part of this work showed that hydrogel porosity and peptide content impacted hS/PC viability and 3D organization. Peptide-modified hydrogels maintained high hS/PC viability and yielded larger multicellular structures that better resembled a developing salivary gland. Use of an integrin ligand led to a higher number of multicellular structures and enhanced hS/PC proliferation. Specifically, migration-permissive (MP-HA) hydrogels led to the highest activation of integrin β1. In short, these experiments defined a hydrogel parameter space for hS/PC encapsulation and 3D culture that avoids confined, spheroidal multicellular assemblies in favor of asymmetric structures with early peripheral buds. Such features bring the models closer to the observed behavior of branching epithelial buds during salivary morphogenesis. The second part of this work describes the isolation and characterization of human salivary-derived fibroblasts (hSFs), and their implementation in co-culture with hS/PCs. hSF-hS/PC 3D encapsulations were conducted either as fully mixed co-cultures, or as adjacent but discrete bilayers. Mixed co-cultures led to significantly higher overall cell viability and structure formation than discrete bilayer co-cultures and monocultures of either cell types. hSFs expressed basement membrane proteins in mixed co-cultures; basement membrane accumulated most in between single hSFs and multicellular hS/PC structures. Lastly, time-lapse imaging of mixed co-cultures illustrated that single cells and multicellular structures composed of either or both cell types were dynamically migrating and reorganizing in MP-HA over time. Thus, the use of MP-HA and a mesenchymal cell type enhanced overall cell viability, growth, and organization in a salivary gland regeneration model. Advisors/Committee Members: Harrington, Daniel A (advisor).

Subjects/Keywords: tissue engineering; hydrogels; hyaluronic acid; salivary gland; cancer; branching morphogenesis

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

APA (6^th Edition):

Martinez, M. (2019). Role of cell-extracellular matrix interactions on tissue morphology, cell phenotype and organization in a salivary gland regeneration model. (Doctoral Dissertation). Rice University. Retrieved from http://hdl.handle.net/1911/105941

Chicago Manual of Style (16^th Edition):

Martinez, Mariane. “Role of cell-extracellular matrix interactions on tissue morphology, cell phenotype and organization in a salivary gland regeneration model.” 2019. Doctoral Dissertation, Rice University. Accessed February 27, 2021. http://hdl.handle.net/1911/105941.

MLA Handbook (7^th Edition):

Martinez, Mariane. “Role of cell-extracellular matrix interactions on tissue morphology, cell phenotype and organization in a salivary gland regeneration model.” 2019. Web. 27 Feb 2021.

Vancouver:

Martinez M. Role of cell-extracellular matrix interactions on tissue morphology, cell phenotype and organization in a salivary gland regeneration model. [Internet] [Doctoral dissertation]. Rice University; 2019. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1911/105941.

Council of Science Editors:

Martinez M. Role of cell-extracellular matrix interactions on tissue morphology, cell phenotype and organization in a salivary gland regeneration model. [Doctoral Dissertation]. Rice University; 2019. Available from: http://hdl.handle.net/1911/105941

University of Pennsylvania

7. Kadzik, Rachel S. Epithelial Cell Shape Changes During Lung Branching Morphogenesis: The Role of Wnt/Fzd2 signaling in directing new branch formation.

Degree: 2014, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/1323

► Formation of the intricately branched mammalian lung requires precise coordination between the epithelium and mesenchyme over the course of development. This coordination is mediated by… (more)

Subjects/Keywords: Branching; Epithelial; Fzd2; Lung; Morphogenesis; Wnt; Cell Biology; Developmental Biology

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APA (6^th Edition):

Kadzik, R. S. (2014). Epithelial Cell Shape Changes During Lung Branching Morphogenesis: The Role of Wnt/Fzd2 signaling in directing new branch formation. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/1323

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):

Kadzik, Rachel S. “Epithelial Cell Shape Changes During Lung Branching Morphogenesis: The Role of Wnt/Fzd2 signaling in directing new branch formation.” 2014. Thesis, University of Pennsylvania. Accessed February 27, 2021. https://repository.upenn.edu/edissertations/1323.

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

MLA Handbook (7^th Edition):

Kadzik, Rachel S. “Epithelial Cell Shape Changes During Lung Branching Morphogenesis: The Role of Wnt/Fzd2 signaling in directing new branch formation.” 2014. Web. 27 Feb 2021.

Vancouver:

Kadzik RS. Epithelial Cell Shape Changes During Lung Branching Morphogenesis: The Role of Wnt/Fzd2 signaling in directing new branch formation. [Internet] [Thesis]. University of Pennsylvania; 2014. [cited 2021 Feb 27]. Available from: https://repository.upenn.edu/edissertations/1323.

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

Council of Science Editors:

Kadzik RS. Epithelial Cell Shape Changes During Lung Branching Morphogenesis: The Role of Wnt/Fzd2 signaling in directing new branch formation. [Thesis]. University of Pennsylvania; 2014. Available from: https://repository.upenn.edu/edissertations/1323

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

8. Havrilak, Jamie Ann. The role of endothelial cells during lung organogenesis.

Degree: PhD, Medicine: Molecular and Developmental Biology, 2015, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1428065611

► Early respiratory development begins with the specification of the lung cell fate, followed by the emergence of lung buds from the ventral foregut endoderm. The… (more)

▼ Early respiratory development begins with the specification of the lung cell fate, followed by the emergence of lung buds from the ventral foregut endoderm. The respiratory tree is then elaborated through branching morphogenesis, and proliferation and differentiation of specialized cell types along the proximal-distal axis produces airways and alveoli, respectively. Lung development is orchestrated through crosstalk between the epithelium and mesenchyme; morphogenesis and differentiation of the lung relies on diffusible signaling molecules that cross tissue layers to activate a complex network of transcription factors to drive development. Significant progress has been made in understanding the molecular regulation of lung morphogenesis through paracrine signaling pathways and transcription factors essential for lung development. The lung mesenchyme is comprised of multiple cell types, however, and which of the mesenchymal cell types are producing these molecules that drive epithelial morphogenesis remains unknown. To determine if endothelial cells are required for epithelial branching morphogenesis we cultured E12.5 lung explants in the presence of 3 different VEGFR inhibitors, which and found epithelial branching was not repressed. We additionally recombined isolated E12.5 lung epithelium (LgE) with mesenchyme from which the endothelial cells had been removed, and found that LgE still branched when cultured with the endothelial cell-depleted mesenchyme. Additionally, we found that LgE did not branch when cultured with human lung microvascular endothelial cells or mouse primary endothelial cells. These data demonstrate that endothelial cells are neither necessary nor sufficient to induce epithelial branching morphogenesis in vitro. To determine if endothelial cells are required for respiratory specification and lung bud initiation, we examined lung formation in E8.5 wild-type embryos cultured in the presence of VEGFR inhibitors and found that specification still occurred when endothelial cell signaling was hindered. However, several caveats to these experiments led us to further investigate this process by utilizing a genetic mouse model in which embryos do not develop a vascular system due to a mutation in the VEGF receptor Flk-1. Due to the decreased size and ultimate embryonic lethality as a result of the Flk-1 mutation, we conducted in vitro foregut culture experiments at E8.5, when wild-type and Flk-1-/- mutant embryos were indistinguishable. As visualized by whole mount confocal microscopy, we found that cultured E8.5 Flk-1-/- mutants expressed Nkx2.1 (a marker for respiratory progenitor cells) in the prospective lung field endoderm to the same extent as wild type littermates, and initiated lung bud formation (measured by SP-C expression), demonstrating that endothelial cells are not necessary for lung specification and bud initiation in vitro.These data collectively suggest that early events in lung organogenesis, such as specification, bud initiation, and terminal branching are not dependent on endothelial… Advisors/Committee Members: Shannon, John (Committee Chair).

Subjects/Keywords: Developmental Biology; Lung; Tissue interactions; Branching morphogenesis; Endothelial cells; Specification

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

APA (6^th Edition):

Havrilak, J. A. (2015). The role of endothelial cells during lung organogenesis. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1428065611

Chicago Manual of Style (16^th Edition):

Havrilak, Jamie Ann. “The role of endothelial cells during lung organogenesis.” 2015. Doctoral Dissertation, University of Cincinnati. Accessed February 27, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1428065611.

MLA Handbook (7^th Edition):

Havrilak, Jamie Ann. “The role of endothelial cells during lung organogenesis.” 2015. Web. 27 Feb 2021.

Vancouver:

Havrilak JA. The role of endothelial cells during lung organogenesis. [Internet] [Doctoral dissertation]. University of Cincinnati; 2015. [cited 2021 Feb 27]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1428065611.

Council of Science Editors:

Havrilak JA. The role of endothelial cells during lung organogenesis. [Doctoral Dissertation]. University of Cincinnati; 2015. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1428065611

Universiteit Utrecht

9. Cheng, O.H. Transcriptional regulation of Drosophila tracheal and neural development.

Degree: 2009, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/31925

► Drosophila melanogaster is an ideal system for investigating the functions of genes and is one of the predominant models for the study of branching morphogenesis… (more)

Subjects/Keywords: Geneeskunde; Drosophila, transcription factor, transciptional regulation, CNS, tracheal system, branching morphogenesis, gene expression, development

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

APA (6^th Edition):

Cheng, O. H. (2009). Transcriptional regulation of Drosophila tracheal and neural development. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/31925

Chicago Manual of Style (16^th Edition):

Cheng, O H. “Transcriptional regulation of Drosophila tracheal and neural development.” 2009. Masters Thesis, Universiteit Utrecht. Accessed February 27, 2021. http://dspace.library.uu.nl:8080/handle/1874/31925.

MLA Handbook (7^th Edition):

Cheng, O H. “Transcriptional regulation of Drosophila tracheal and neural development.” 2009. Web. 27 Feb 2021.

Vancouver:

Cheng OH. Transcriptional regulation of Drosophila tracheal and neural development. [Internet] [Masters thesis]. Universiteit Utrecht; 2009. [cited 2021 Feb 27]. Available from: http://dspace.library.uu.nl:8080/handle/1874/31925.

Council of Science Editors:

Cheng OH. Transcriptional regulation of Drosophila tracheal and neural development. [Masters Thesis]. Universiteit Utrecht; 2009. Available from: http://dspace.library.uu.nl:8080/handle/1874/31925

McMaster University

10. Sarin, Sanjay. β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis.

Degree: MSc, 2013, McMaster University

URL: http://hdl.handle.net/11375/12888

►

Renal dysplasia, a developmental disorder characterized by defective nephrogenesis and branching morphogenesis, ranks as one of the major causes of renal failure among the… (more)

▼

Renal dysplasia, a developmental disorder characterized by defective nephrogenesis and branching morphogenesis, ranks as one of the major causes of renal failure among the pediatric population. The molecular mechanisms underlying the pathogenesis of renal dysplasia are not well understood; however, changes in gene expression are a major contributing factor. In this study, we demonstrate that the levels of activated β-catenin, a transcriptional co-regulator, are elevated in the nuclei of ureteric, stromal, and mesenchymal cells within dysplastic human kidney tissue. To determine the mechanisms by which mesenchymal β-catenin over-expression leads to renal dysplasia, we generated a conditional mouse model in which β-catenin was stabilized exclusively in the metanephric mesenchyme. Kidneys from these mutant mice are remarkably similar to dysplastic human kidneys. In addition, these mutant mice also demonstrate the formation of 4 to 6 ectopic kidneys. While nephrogenesis appeared normal, investigation of ureteric branch pattern revealed ectopic ureteric budding off the Wolffian duct, ectopic branching off the initial ureteric bud stalk and a disorganization of branch patterning. In-situ hybridization of mutant kidneys revealed increased expression of Gdnf, Cret, and Wnt11, key factors that regulate ureteric branch patterning. We further demonstrate that β-catenin directly binds to TCF consensus binding sites within the Gdnf promoter region located 4.9kb, 2.25kb and 2.1kb upstream of the Gdnf transcriptional start site. Molecular cloning of the 4.9kb fragment upstream of a luciferase gene revealed that ß-catenin regulates gene transcription from the 4.9kb consensus site. Consistent with these findings, genetic deletion of β-catenin from the metanephric mesenchyme cell lineage lead to decreased Gdnf expression and a reduction in ureteric branching morphogenesis resulting in renal hypoplasia. Taken together, our findings establish that β-catenin is an essential regulator of Gdnf expression within the metanephric mesenchyme. Furthermore, we have identified a novel disrupted signalling pathway that contributes to the pathogenesis of renal dysplasia. In this pathway, an over-expression of β-catenin directly leads to an over-expression of Gdnf, causing ectopic and disorganized branching morphogenesis and, consequently, renal dysplasia.

Master of Health Sciences (MSc)

Advisors/Committee Members: Bridgewater, Darren, Medical Sciences.

Subjects/Keywords: Kidney development; branching morphogenesis; Developmental Biology; Genetic Processes; Medical Sciences; Developmental Biology

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APA (6^th Edition):

Sarin, S. (2013). β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/12888

Chicago Manual of Style (16^th Edition):

Sarin, Sanjay. “β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis.” 2013. Masters Thesis, McMaster University. Accessed February 27, 2021. http://hdl.handle.net/11375/12888.

MLA Handbook (7^th Edition):

Sarin, Sanjay. “β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis.” 2013. Web. 27 Feb 2021.

Vancouver:

Sarin S. β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis. [Internet] [Masters thesis]. McMaster University; 2013. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/11375/12888.

Council of Science Editors:

Sarin S. β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis. [Masters Thesis]. McMaster University; 2013. Available from: http://hdl.handle.net/11375/12888

University of Toronto

11. Kablawi, Dana. Functional Consequence of Human Missense Variants in Integrin-linked Kinase on Renal Branching Morphogenesis.

Degree: 2018, University of Toronto

URL: http://hdl.handle.net/1807/101600

►

Mammalian kidney function depends on the presence of a critical complement of nephrons connected to an intact collecting system. Malformation of these elements is characteristic… (more)

Subjects/Keywords: hypoplasia; Integrin-linked kinase; MAPK; missense variants; renal branching morphogenesis; ureteric bud; 0369

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APA (6^th Edition):

Kablawi, D. (2018). Functional Consequence of Human Missense Variants in Integrin-linked Kinase on Renal Branching Morphogenesis. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/101600

Chicago Manual of Style (16^th Edition):

Kablawi, Dana. “Functional Consequence of Human Missense Variants in Integrin-linked Kinase on Renal Branching Morphogenesis.” 2018. Masters Thesis, University of Toronto. Accessed February 27, 2021. http://hdl.handle.net/1807/101600.

MLA Handbook (7^th Edition):

Kablawi, Dana. “Functional Consequence of Human Missense Variants in Integrin-linked Kinase on Renal Branching Morphogenesis.” 2018. Web. 27 Feb 2021.

Vancouver:

Kablawi D. Functional Consequence of Human Missense Variants in Integrin-linked Kinase on Renal Branching Morphogenesis. [Internet] [Masters thesis]. University of Toronto; 2018. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1807/101600.

Council of Science Editors:

Kablawi D. Functional Consequence of Human Missense Variants in Integrin-linked Kinase on Renal Branching Morphogenesis. [Masters Thesis]. University of Toronto; 2018. Available from: http://hdl.handle.net/1807/101600

University of Oxford

12. Yates, Laura Louise. The role of the planar cell polarity pathway in branching morphogenesis.

Degree: PhD, 2011, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:65200972-a024-4b68-bfd3-a857ec8d99d8 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534016

► The development of organs such as the lung and kidney occurs by branching morphogenesis. Changes in the cytoskeletal architecture, cell-cell adhesion and cell polarity are… (more)

▼ The development of organs such as the lung and kidney occurs by branching morphogenesis. Changes in the cytoskeletal architecture, cell-cell adhesion and cell polarity are necessary for the formation of new branches. Interactions and reciprocal signalling between epithelial and mesenchymal cells mediate these organised cell movements that give rise to a complex system of tubes suitable for the transport of gas or fluids. Mutations that disrupt formation of either the correct number, or shape of epithelial branches, affect lung function. This, in turn, can lead to congenital abnormalities such as cystadenomatoid malformations, pulmonary hypertension or lung hypoplasia. Defects in lung architecture are also associated with adult lung disease, particularly in cases of idiopathic lung ﬁbrosis. Identifying the signaling pathways that drive epithelial tube formation will likely shed light on both congenital and adult lung disease. This study shows that mutations in the planar cell polarity (PCP) genes: Celsr1; Vangl2 and Scribble, lead to disrupted lung development and defects in lung architecture. Examination of Vangl2 mutant kidneys reveals similar impairment of branching morphogenesis. Detailed histological and immunocytochemical analysis reveals that lungs from Celsr1Crsh/Crsh, Vangl2Lp/Lp and ScribbleCrc/Crc mice are small and misshapen with fewer branches, and by late gestation exhibit thickened interstitial mesenchyme and defective saccular formation. Moreover, epithelial integrity is disrupted, cytoskeletal remodeling perturbed and mutant endoderm does not branch normally in response to the chemoattractant FGF10. In ex-vivo culture, inhibition of Rho kinase, an important downstream effector of the PCP signaling pathway, can mimic the branching defects observed in these three mouse mutants. Furthermore, all three proteins are present in restricted spatial domains within lung epithelium. ScribbleCrc/Crc lungs, the most severely affected line, exhibit additional defects in components of the tight and adherens junctions; this in turn affects lumen diameter. These findings show that components of the PCP pathway: Celsr1; Vangl2 and Scribble are required for normal foetal lung development, thereby revealing a novel signalling pathway critical for this process. Examination of postnatal mice was not possible as homozygous mutations result in embryonic lethality. However, an assessment of Vangl2Lp/+ mice reveals that loss of a single copy of Vangl2 is enough to cause defects in embryonic lung development that persist into adult life, affecting lung function. Similarly, Vangl2Lp/+ mice show a small but significant reduction in kidney glomeruli.

Subjects/Keywords: 612.2; Biochemistry; Genetics (life sciences); Development (zoology); Lung Development; Planar Cell Polarity; Branching Morphogenesis

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

APA (6^th Edition):

Yates, L. L. (2011). The role of the planar cell polarity pathway in branching morphogenesis. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:65200972-a024-4b68-bfd3-a857ec8d99d8 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534016

Chicago Manual of Style (16^th Edition):

Yates, Laura Louise. “The role of the planar cell polarity pathway in branching morphogenesis.” 2011. Doctoral Dissertation, University of Oxford. Accessed February 27, 2021. http://ora.ox.ac.uk/objects/uuid:65200972-a024-4b68-bfd3-a857ec8d99d8 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534016.

MLA Handbook (7^th Edition):

Yates, Laura Louise. “The role of the planar cell polarity pathway in branching morphogenesis.” 2011. Web. 27 Feb 2021.

Vancouver:

Yates LL. The role of the planar cell polarity pathway in branching morphogenesis. [Internet] [Doctoral dissertation]. University of Oxford; 2011. [cited 2021 Feb 27]. Available from: http://ora.ox.ac.uk/objects/uuid:65200972-a024-4b68-bfd3-a857ec8d99d8 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534016.

Council of Science Editors:

Yates LL. The role of the planar cell polarity pathway in branching morphogenesis. [Doctoral Dissertation]. University of Oxford; 2011. Available from: http://ora.ox.ac.uk/objects/uuid:65200972-a024-4b68-bfd3-a857ec8d99d8 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.534016

Princeton University

13. Piotrowski-Daspit, Alexandra Sarah Annukka. Physical Forces and Collective Cell Migration in Development and Disease .

Degree: PhD, 2016, Princeton University

URL: http://arks.princeton.edu/ark:/88435/dsp016108vd67j

► Collective cell migration is a key driver of tissue remodeling during development, wound healing, and cancer invasion. However, the mechanisms cells employ to move cohesively… (more)

▼ Collective cell migration is a key driver of tissue remodeling during development, wound healing, and cancer invasion. However, the mechanisms cells employ to move cohesively and the influence of the physical microenvironment on collective behavior have not been fully elucidated. Using two different engineered three-dimensional (3D) culture models, we show that cells require mechanical sensing to migrate collectively and that extrinsic physical forces in their microenvironment can influence the migratory phenotype. We conclude that physical forces and biomechanics play a vital role in collective migration, both in development and disease contexts. To study the physical mechanisms of collective migration in mammary gland branching morphogenesis, we used 3D engineered tissues embedded in collagen, a fibrous extracellular matrix (ECM) protein found in the natural cellular microenvironment. We show directly and quantitatively that collective migration occurs via a dynamic pulling mechanism, with pericellular matrix alignment preceding translocation. Tensile forces increase at the invasive front of cohorts, serving a physical role and a regulatory one by conditioning the cells and matrix for further extension. These forces elicit mechanosensitive signaling within the leading edge and align the ECM, creating microtracks critical for migration. Cell movements are highly correlated and in phase with ECM deformations. Migrating cohorts use spatially localized, long-range forces and consequent matrix alignment to navigate the ECM. We also determined how an extrinsic physical force in the microenvironment of solid tumors, elevated interstitial fluid pressure (IFP), influences collective cancer invasion. Elevated IFP is a characteristic feature of solid tumors; IFP rises steeply beyond the tumor periphery and plateaus at values as high as 50 mm Hg above a normal value of 0 mm Hg, resulting in outward fluid flow from the tumor core towards the periphery. We used a 3D engineered model of a human breast tumor to probe the effects of IFP on collective invasion. We found that IFP influences the motility and invasive behavior of cancer cells by regulating the expression of genes associated with migratory behavior (epithelial-mesenchymal transition (EMT) genes). The expression levels of these markers are both necessary and sufficient to drive invasive behavior in response to IFP. Advisors/Committee Members: Nelson, Celeste M (advisor).

Subjects/Keywords: Branching Morphogenesis; Collective Cell Migration; Extracellular Matrix Remodeling; Interstitial Fluid Pressure; Mechanical Stress; Morphodynamics

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APA (6^th Edition):

Piotrowski-Daspit, A. S. A. (2016). Physical Forces and Collective Cell Migration in Development and Disease . (Doctoral Dissertation). Princeton University. Retrieved from http://arks.princeton.edu/ark:/88435/dsp016108vd67j

Chicago Manual of Style (16^th Edition):

Piotrowski-Daspit, Alexandra Sarah Annukka. “Physical Forces and Collective Cell Migration in Development and Disease .” 2016. Doctoral Dissertation, Princeton University. Accessed February 27, 2021. http://arks.princeton.edu/ark:/88435/dsp016108vd67j.

MLA Handbook (7^th Edition):

Piotrowski-Daspit, Alexandra Sarah Annukka. “Physical Forces and Collective Cell Migration in Development and Disease .” 2016. Web. 27 Feb 2021.

Vancouver:

Piotrowski-Daspit ASA. Physical Forces and Collective Cell Migration in Development and Disease . [Internet] [Doctoral dissertation]. Princeton University; 2016. [cited 2021 Feb 27]. Available from: http://arks.princeton.edu/ark:/88435/dsp016108vd67j.

Council of Science Editors:

Piotrowski-Daspit ASA. Physical Forces and Collective Cell Migration in Development and Disease . [Doctoral Dissertation]. Princeton University; 2016. Available from: http://arks.princeton.edu/ark:/88435/dsp016108vd67j

University of Rochester

14. Wang, Qiong. Regulatory Interactions between Fibroblast Growth Factor, a Matrix Metalloproteinase and a Proteoglycan in the Control of Branching Morphogenesis.

Degree: PhD, 2010, University of Rochester

URL: http://hdl.handle.net/1802/11845

► Fibroblast Growth Factor (FGF) is a central regulator of branching morphogenesis processes, such as angiogenesis or the development of branched organs including lung, kidney and… (more)

Subjects/Keywords: Matrix Metalloproteinase (MMP); Fibroblast Growth Factor (FGF); Heparin Sulfate Proteoglycon (HSPG); Branching Morphogenesis

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APA (6^th Edition):

Wang, Q. (2010). Regulatory Interactions between Fibroblast Growth Factor, a Matrix Metalloproteinase and a Proteoglycan in the Control of Branching Morphogenesis. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/11845

Chicago Manual of Style (16^th Edition):

Wang, Qiong. “Regulatory Interactions between Fibroblast Growth Factor, a Matrix Metalloproteinase and a Proteoglycan in the Control of Branching Morphogenesis.” 2010. Doctoral Dissertation, University of Rochester. Accessed February 27, 2021. http://hdl.handle.net/1802/11845.

MLA Handbook (7^th Edition):

Wang, Qiong. “Regulatory Interactions between Fibroblast Growth Factor, a Matrix Metalloproteinase and a Proteoglycan in the Control of Branching Morphogenesis.” 2010. Web. 27 Feb 2021.

Vancouver:

Wang Q. Regulatory Interactions between Fibroblast Growth Factor, a Matrix Metalloproteinase and a Proteoglycan in the Control of Branching Morphogenesis. [Internet] [Doctoral dissertation]. University of Rochester; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1802/11845.

Council of Science Editors:

Wang Q. Regulatory Interactions between Fibroblast Growth Factor, a Matrix Metalloproteinase and a Proteoglycan in the Control of Branching Morphogenesis. [Doctoral Dissertation]. University of Rochester; 2010. Available from: http://hdl.handle.net/1802/11845

Vanderbilt University

15. Zhang, Xi. Beta1 integrin in kidney development.

Degree: PhD, Cancer Biology, 2010, Vanderbilt University

URL: http://hdl.handle.net/1803/11109

► The major goal of this thesis is to examine the role of beta1 integrin in kidney development. Our results indicate that beta1 integrin is necessary… (more)

Subjects/Keywords: kidney development; branching morphogenesis; integrin; UUO; glomerular filtration barrier; growth factor; podocyte

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APA (6^th Edition):

Zhang, X. (2010). Beta1 integrin in kidney development. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11109

Chicago Manual of Style (16^th Edition):

Zhang, Xi. “Beta1 integrin in kidney development.” 2010. Doctoral Dissertation, Vanderbilt University. Accessed February 27, 2021. http://hdl.handle.net/1803/11109.

MLA Handbook (7^th Edition):

Zhang, Xi. “Beta1 integrin in kidney development.” 2010. Web. 27 Feb 2021.

Vancouver:

Zhang X. Beta1 integrin in kidney development. [Internet] [Doctoral dissertation]. Vanderbilt University; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1803/11109.

Council of Science Editors:

Zhang X. Beta1 integrin in kidney development. [Doctoral Dissertation]. Vanderbilt University; 2010. Available from: http://hdl.handle.net/1803/11109

16. Razetti, Agustina. Modélisation et caractérisation de la croissance des axones à partir de données in vivo : Modelling and characterizing axon growth from in vivo data.

Degree: Docteur es, Automatique, traitement du signal et des images, 2018, Université Côte d'Azur (ComUE)

URL: http://www.theses.fr/2018AZUR4016

►

La construction du cerveau et de ses connexions pendant le développement reste une question ouverte dans la communauté scientifique. Des efforts fructueux ont été faits… (more)

▼

La construction du cerveau et de ses connexions pendant le développement reste une question ouverte dans la communauté scientifique. Des efforts fructueux ont été faits pour élucider les mécanismes de la croissance axonale, tels que la guidance axonale et les molécules de guidage. Cependant, des preuves récentes suggèrent que d'autres acteurs seraient impliqués dans la croissance des neurones in vivo. Notamment, les axones se développent dans des environnements mécaniquement contraints. Ainsi, pour bien comprendre ce processus dynamique, il faut prendre en compte les mécanismes collectifs et les interactions mécaniques au sein des populations axonales. Néanmoins, les techniques pour mesurer directement cela à partir de cerveaux vivants sont aujourd'hui insuffisantes ou lourdes à mettre en œuvre. Cette thèse résulte d'une collaboration multidisciplinaire, pour faire la lumière sur le développement axonal in vivo et les morphologies complexes des axones adultes. Notre travail a été inspiré et validé à partir d'images d'axones y individuels chez la drosophile, de type sauvage et modifiés génétiquement, que nous avons segmentés et normalisés. Nous avons d'abord proposé un cadre mathématique pour l'étude morphologique et la classification des groupes axonaux. A partir de cette analyse, nous avons émis l'hypothèse que la croissance axonale dérive d'un processus stochastique et que la variabilité et la complexité des arbres axonaux résultent de sa nature intrinsèque, ainsi que des stratégies d'élongation développées pour surmonter les contraintes mécaniques du cerveau en développement. Nous avons conçu un modèle mathématique de la croissance d'un axone isolé fondé sur des chaînes de Markov gaussiennes avec deux paramètres, représentant la rigidité axonale et l'attraction du champ cible. Nous avons estimé les paramètres de ce modèle à partir de données réelles et simulé la croissance des axones à l'échelle de populations et avec des contraintes spatiales pour tester notre hypothèse. Nous avons abordé des thèmes de mathématiques appliquées ainsi que de la biologie, et dévoilé des effets inexplorés de la croissance collective sur le développement axonal in vivo.

How the brain wires up during development remains an open question in the scientific community across disciplines. Fruitful efforts have been made to elucidate the mechanisms of axonal growth, such as pathfinding and guiding molecules. However, recent evidence suggests other actors to be involved in neuron growth in vivo. Notably, axons develop in populations and embedded in mechanically constrained environments. Thus, to fully understand this dynamic process, one must take into account collective mechanisms and mechanical interactions within the axonal populations. However, techniques to directly measure this from living brains are today lacking or heavy to implement. This thesis emerges from a multidisciplinary collaboration, to shed light on axonal development in vivo and how adult complex axonal morphologies are attained. Our work is inspired and validated from…

Advisors/Committee Members: Descombes, Xavier (thesis director).

Subjects/Keywords: Croissance axonale; Morphogenèse; Modélisation stochastique; Chaînes de Markov gaussiennes; Interactions mécaniques; Ramification axonale; Stratégies d'élongation; Axon growth; Morphogenesis; Stochastic modelling; Gaussian markov chains; Mechanical interactions; Axon branching; Elongation strategies

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

APA (6^th Edition):

Razetti, A. (2018). Modélisation et caractérisation de la croissance des axones à partir de données in vivo : Modelling and characterizing axon growth from in vivo data. (Doctoral Dissertation). Université Côte d'Azur (ComUE). Retrieved from http://www.theses.fr/2018AZUR4016

Chicago Manual of Style (16^th Edition):

Razetti, Agustina. “Modélisation et caractérisation de la croissance des axones à partir de données in vivo : Modelling and characterizing axon growth from in vivo data.” 2018. Doctoral Dissertation, Université Côte d'Azur (ComUE). Accessed February 27, 2021. http://www.theses.fr/2018AZUR4016.

MLA Handbook (7^th Edition):

Razetti, Agustina. “Modélisation et caractérisation de la croissance des axones à partir de données in vivo : Modelling and characterizing axon growth from in vivo data.” 2018. Web. 27 Feb 2021.

Vancouver:

Razetti A. Modélisation et caractérisation de la croissance des axones à partir de données in vivo : Modelling and characterizing axon growth from in vivo data. [Internet] [Doctoral dissertation]. Université Côte d'Azur (ComUE); 2018. [cited 2021 Feb 27]. Available from: http://www.theses.fr/2018AZUR4016.

Council of Science Editors:

Razetti A. Modélisation et caractérisation de la croissance des axones à partir de données in vivo : Modelling and characterizing axon growth from in vivo data. [Doctoral Dissertation]. Université Côte d'Azur (ComUE); 2018. Available from: http://www.theses.fr/2018AZUR4016

University of Cincinnati

17. METZGER, DAVID EDWARD. THE ROLE OF THE ETS TRANSCRIPTION FACTOR Elf5 IN LUNG DEVELOPMENT.

Degree: PhD, Medicine : Molecular and Developmental Biology, 2007, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1197664589

► Epithelial FGF signaling during lung organogenesis has been shown to be essential for branching morphogenesis, specification of surfactant producing type II cells and the maintenance… (more)

▼ Epithelial FGF signaling during lung organogenesis has been shown to be essential for branching morphogenesis, specification of surfactant producing type II cells and the maintenance of epithelial progenitors. In order to determine epithelial targets of FGF signaling, E11.5 mouse lungs were cultured for 24 hours in the presence of the FGF receptor antagonist SU5402, which inhibited branching morphogenesis. Affymetrix gene chip analysis identified a number of epithelial genes regulated by FGF signaling, including Elf5, a member of the Epithelial Specific Ets family of transcription factors. In situ hybridization revealed that Elf5 had a dynamic pattern of expression during lung development, transitioning from the distal epithelium at E11.5 to the proximal airway epithelium in late lung development. It was also determined that expression of Elf5 was induced by FGF7 and FGF10, ligands of epithelial specific FGFR2b. In order to further define the pathways by which FGFs activate Elf5 expression, E11.5 lung tips were also cultured in the presence of inhibitors of PI3-Kinase/Akt-mediated signaling (LY294002) and MAP Kinase/Erk-mediated signaling (U0126). It was found that LY294002 significantly reduced Elf5 expression, whereas U0126 had no effect. The observation that proximal airway epithelium (a tissue that lacks expression of distal epithelial markers) highly expressed Elf5 in late gestation suggested that Elf5 may play a role in negatively regulating distal epithelial specification/differentiation. To test this hypothesis, a transgenic mouse model was generated containing a doxycycline inducible HA-tagged Elf5 transgene under the control of the lung epithelium specific Sftpc promoter to overexpress Elf5 in the distal lung epithelium. The results indicated that high Elf5 expression disrupted branching morphogenesis and negatively regulated distal epithelial differentiation of the lung epithelium while repressing type II cell enriched genes Erm, Napsin and Sftpc. Furthermore, microarray analysis of Elf5 overexpressing lungs revealed that while repressing some genes normally present in differentiated type II cells, high Elf5 expression also induced the expressions of other genes present in type II cells, suggesting that appropriate levels of Elf5 expression must be regulated for the proper specification and the subsequent differentiation of type II cells. Further analysis of the microarray results indicated that Elf5 overexpression induced the ectopic expressions of genes not normally associated with the lung. These results suggest that high Elf5 expression in the lung epithelium plays a role in negatively regulating the specification and differentiation of type II cells but may also play a role in keeping the lung epithelium somewhat pluripotent. Advisors/Committee Members: Shannon, Dr. John (Advisor).

Subjects/Keywords: Lung Development; Branching Morphogenesis; FGF-Signaling; Epithelial Differentiation; Elf5; ETS

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APA (6^th Edition):

METZGER, D. E. (2007). THE ROLE OF THE ETS TRANSCRIPTION FACTOR Elf5 IN LUNG DEVELOPMENT. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1197664589

Chicago Manual of Style (16^th Edition):

METZGER, DAVID EDWARD. “THE ROLE OF THE ETS TRANSCRIPTION FACTOR Elf5 IN LUNG DEVELOPMENT.” 2007. Doctoral Dissertation, University of Cincinnati. Accessed February 27, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1197664589.

MLA Handbook (7^th Edition):

METZGER, DAVID EDWARD. “THE ROLE OF THE ETS TRANSCRIPTION FACTOR Elf5 IN LUNG DEVELOPMENT.” 2007. Web. 27 Feb 2021.

Vancouver:

METZGER DE. THE ROLE OF THE ETS TRANSCRIPTION FACTOR Elf5 IN LUNG DEVELOPMENT. [Internet] [Doctoral dissertation]. University of Cincinnati; 2007. [cited 2021 Feb 27]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1197664589.

Council of Science Editors:

METZGER DE. THE ROLE OF THE ETS TRANSCRIPTION FACTOR Elf5 IN LUNG DEVELOPMENT. [Doctoral Dissertation]. University of Cincinnati; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1197664589

University of Toronto

18. Rutter, Martin Edward. GLI2 Transcriptional Cascade During Mouse Fetal Lung Development.

Degree: 2008, University of Toronto

URL: http://hdl.handle.net/1807/11255

►

The lung is an organ that contains a vast system of airways carefully constructed to achieve maximal surface area in a confined space, requiring guidance… (more)

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The lung is an organ that contains a vast system of airways carefully constructed to achieve maximal surface area in a confined space, requiring guidance from a multitude of developmental factors. The Shh pathway is one such signaling mechanism that is critical to proper lung formation, guiding branching morphogenesis and cellular proliferation through its downstream Gli transcription factors. Additionally, Foxf1 has been shown to be a key developmental factor required for proper lung formation during embryogenesis. Although theorized that the Gli transcription factors are responsible for regulating foxf1 levels, their exact relationship has yet to be revealed. Using five different models for Shh signaling (gli2 null, gli2 over-expressor [hVER-Gli2], gli3 null, Gli3 constitutive repressor [Gli3Δ699] and cyclopamine treated lung explants), I compared and contrasted the role of Gli2 and Gli3 in terms of their effect on cell cycle regulation, and on the expression levels of foxf1 and its potential downstream target genes tbx4, tbx5 and fgf10. I found that ectopic over-expression of gli2 resulted in increased Shh pathway activation, and increased expression of G1/S phase cyclins, which was associated with increased cellular proliferation and lung growth. However, no change in the levels of G1/S phase cyclins due to altered Gli3 signaling was observed. Foxf1 levels positively correlate with the levels of gli2, and appear to be independent of Gli3 activity. The amount of tbx4, tbx5, and fgf10 transcripts were observed to follow the levels of gli2 in the different gli2 mouse models, however, there was no significant change in gli3 null or Gli3Δ699 mice. Finally, by analyzing gene expression at different time points during gestation, I found that while gli2 levels affect foxf1 throughout gestation, the relationship to tbx4, tbx5 and fgf10, occurs only during the latter stages of lung development. I conclude, that Gli2 and not Gli3 appears to be the primary transducer of Shh signaling influencing cyclin regulation, leading to changes in embryonic lung growth. Furthermore, that Gli2 and not Gli3 appears to regulate foxf1 expression levels, and that this may extend downstream to influence tbx4, tbx5 and fgf10 expression.

PhD

Advisors/Committee Members: Post, Martin, Medical Science.

Subjects/Keywords: Sonic Hedgehog; Gli2; Foxf1; Lung; Pulmonary; Mouse; Transgenic; Development; Gli3; Shh; Cellular Proliferation; Morphogenesis; Fgf10; Branching Morphogenesis; Embryo; Transgene; 0369

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

APA (6^th Edition):

Rutter, M. E. (2008). GLI2 Transcriptional Cascade During Mouse Fetal Lung Development. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/11255

Chicago Manual of Style (16^th Edition):

Rutter, Martin Edward. “GLI2 Transcriptional Cascade During Mouse Fetal Lung Development.” 2008. Doctoral Dissertation, University of Toronto. Accessed February 27, 2021. http://hdl.handle.net/1807/11255.

MLA Handbook (7^th Edition):

Rutter, Martin Edward. “GLI2 Transcriptional Cascade During Mouse Fetal Lung Development.” 2008. Web. 27 Feb 2021.

Vancouver:

Rutter ME. GLI2 Transcriptional Cascade During Mouse Fetal Lung Development. [Internet] [Doctoral dissertation]. University of Toronto; 2008. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1807/11255.

Council of Science Editors:

Rutter ME. GLI2 Transcriptional Cascade During Mouse Fetal Lung Development. [Doctoral Dissertation]. University of Toronto; 2008. Available from: http://hdl.handle.net/1807/11255

19. Feinberg, Tamar Yael. Extracellular Matrix Remodeling and the Control of Branching Morphogenetic Programs.

Degree: PhD, Cellular and Molecular Biology, 2016, University of Michigan

URL: http://hdl.handle.net/2027.42/120758

► Epithelial cells and endothelial cells initiate distinct branching morphogenetic programs during their coordinated invasion and proliferation into the interstitial compartment, a tissue comprised of mesenchymal… (more)

▼ Epithelial cells and endothelial cells initiate distinct branching morphogenetic programs during their coordinated invasion and proliferation into the interstitial compartment, a tissue comprised of mesenchymal stromal cells and extracellular matrix (ECM). While mammary gland development occurs in a specialized stromal environment dominated by adipocytes and fibroblasts, endothelial cell branching proceeds throughout all tissues in the absence of a specific stromal cell population. Nevertheless, both epithelial cells and endothelial cells engaged in morphogenetic responses have been posited to mobilize proteolytic enzymes to penetrate ECM barriers. However, transgenic mouse models have failed to identify required proteolytic effectors or uncover the mechanisms whereby proteolytic changes in tissue microenvironments regulate cell behavior. Herein, we characterize functional roles performed by the two dominant transmembrane proteinases expressed during epithelial and endothelial cell branching processes, the membrane-anchored matrix metalloproteinases, MT1-MMP and MT2-MMP. Using a series of transgenic mouse models, we identify new and unanticipated roles for MT1-MMP and MT2-MMP in mammary gland morphogenesis as well as angiogenesis. Tissue-specific targeting of MT1-MMP and MT2-MMP demonstrate that early mammary gland branching, which takes place within an immature ECM, proceeds independently of either proteinase. Instead, both proteinases play important, but diametrically opposed, roles in mammary gland adipocytes, where MT1-MMP stimulates adipogenesis and lipid metabolism, while MT2-MMP represses the development of thermogenic beige/brown adipocytes. In marked contrast, during the major phases of postnatal mammary gland development where a mature ECM is actively deposited, branching requires stromal cell-, rather than epithelial cell-, derived MT1-MMP, where the proteinase regulates branching by remodeling a periductal network of ECM macromolecules dominated by type I collagen. Endothelial cells also rely on MT1-MMP to direct branching, but unexpectedly, the proteinase also controls proliferative responses via a novel regulatory axis wherein pericellular proteolysis of the ECM governs the cytoskeletal-nuclear membrane interactions responsible for regulating transcriptional activity. Together, these data create new paradigms relevant to morphogenesis and tissue remodeling, as well as identify novel roles for membrane-anchored metalloproteinases in governing ECM proteolysis and associated transcriptional programs. Advisors/Committee Members: Weiss, Stephen J. (committee member), Engel, James Doug (committee member), Fearon, Eric R. (committee member), Guan, Jun-Lin (committee member), Saltiel, Alan R. (committee member).

Subjects/Keywords: Biological Sciences; Developmental Biology; Branching Morphogenesis; Cell Migration; Molecular, Cellular and Developmental Biology; Science

…Branching morphogenesis as a general developmental paradigm. Epithelial and endothelial organ… …networks, processes known as branching morphogenesis and angiogenesis, respectively (Andrew… …coincident with branching morphogenesis drives the formation of the respiratory, circulatory and… …branching morphogenesis in vivo remains undefined. Early evidence implicating cell movement and… …collective cell migrations in branching morphogenesis came from seminal work performed with fruit…

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

APA (6^th Edition):

Feinberg, T. Y. (2016). Extracellular Matrix Remodeling and the Control of Branching Morphogenetic Programs. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/120758

Chicago Manual of Style (16^th Edition):

Feinberg, Tamar Yael. “Extracellular Matrix Remodeling and the Control of Branching Morphogenetic Programs.” 2016. Doctoral Dissertation, University of Michigan. Accessed February 27, 2021. http://hdl.handle.net/2027.42/120758.

MLA Handbook (7^th Edition):

Feinberg, Tamar Yael. “Extracellular Matrix Remodeling and the Control of Branching Morphogenetic Programs.” 2016. Web. 27 Feb 2021.

Vancouver:

Feinberg TY. Extracellular Matrix Remodeling and the Control of Branching Morphogenetic Programs. [Internet] [Doctoral dissertation]. University of Michigan; 2016. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2027.42/120758.

Council of Science Editors:

Feinberg TY. Extracellular Matrix Remodeling and the Control of Branching Morphogenetic Programs. [Doctoral Dissertation]. University of Michigan; 2016. Available from: http://hdl.handle.net/2027.42/120758

20. Katidou, M. Μοριακός χαρακτηρισμός του γονιδίου rig-6: ο ρόλος του στην ανάπτυξη του Caenorhabditis elegans.

Degree: 2010, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/27190

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Immunoglobulin superfamily Cell Adhesion Molecules (IgCAMs) are key regulators of nervous system development. The contactin subgroup of IgCAMs consists of GPIanchoredglycoproteins implicated in axon outgrowth,… (more)

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Immunoglobulin superfamily Cell Adhesion Molecules (IgCAMs) are key regulators of nervous system development. The contactin subgroup of IgCAMs consists of GPIanchoredglycoproteins implicated in axon outgrowth, guidance, fasciculation and neuronal differentiation. The intracellular mechanism by which contactins facilitate neuronal development is not understood. To gain insight into the function of contactins, we characterized RIG-6, the sole contactin of C. elegans. Here, we show that RIG-6 affects longitudinal axon outgrowth of mechanosensory neurons in a cell autonomous manner. Furthermore RIG-6 is implicated in axon guidance along the circumferential axis. We find that RIG-6 facilitates accurate nervous system patterning by prohibiting commissural dendrite convergence and branching, as well as axon cross-over at the ventral nerve cord.RIG-6 expression levels are critical for nervous system architecture. Upregulation of this contactin causes several behavioral deficits such as abnormal locomotion, egg laying and defecation. In addition to its neuronal function, RIG-6 is also involved in nonneuronal cell migration and morphogenesis, affecting Distal Tip Cell migration and excretory canal extension. Our data suggest that RIG-6 and the cytoplasmic protein UNC-53 synergize to directaxon guidance and branching along both the anterior-posterior and dorso-ventral direction. This implies that UNC-53/NAV2 proteins may contribute to relay signaling via contactins.

Η Υπεροικογένεια των Ανοσοσφαιρινών είναι μια πολύ μεγάλη που συντηρούνται εξελικτικά από το νηματώδη ως τον άνθρωπο. Τα μόρια κυτταρικής συνάφειας της υπεροικογένειας αυτής, διαδραματίζουν ιδιαίτερα σημαντικό ρόλο στην ανάπτυξη του νευρικού συστήματος, καθορίζοντας την αύξηση και καθοδήγηση αξόνων, τη μετανάστευση νευρώνων και τη διαφοροποίησή τους. Η υποοικογένεια contactin συνίσταται από πρωτεΐνες που προσδένονται στη μεμβράνη μέσω του λιπιδίου γλυκοζυλ-φωσφατιδυλ-ινοσιτόλη (GPI). Αλληλεπιδρούν με όμοια ή διαφορετικά μόρια που εντοπίζονται στην κυτταρική μεμβράνη και εμπλέκονται σε όλες τις προαναφερθείσες διαδικασίες. Ωστόσο, οι ενδοκυτταρικοί μηχανισμοί δράσης τους δεν είναι κατανοητοί. Με στόχο τη διερεύνηση των μηχανισμών αυτών μελετήσαμε τη μοναδική contactinRIG-6 στο νηματώδη Caenorhabditis elegans. Στην παρούσα διατριβή δείχνουμε ότι τοRIG-6 εμπλέκεται, με κυτταρικά αυτόνομο τρόπο, στην αύξηση των αξόνων των μηχανοαισθητηρίων νευρώνων που συμβαίνει κατά την πρόσθια-οπίσθια κατεύθυνση. Παράλληλα, το RIG-6 επηρεάζει την καθοδήγηση των συνδεσμικών αξόνων των κινητικών νευρώνων της κοιλιακής νευρικής χορδής. Τα επίπεδα έκφρασης του RIG-6είναι ιδιαίτερα κρίσιμα για τη σωστή ανάπτυξη του νευρικού συστήματος. Η υπερέκφραση αυτής της contactin προκαλεί τη συνένωση και δημιουργία βρόγχων των συνδεσμικών αξόνων. Οι διαταραχές που προκαλούνται από την αύξηση των επιπέδων του μορίου επηρεάζουν συγκεκριμένες συμπεριφορές του νηματώδους όπως η κίνηση, η εναπόθεση αυγών και η απέκκριση. Επιπρόσθετα, το RIG-6 σχετίζεται με τη μετανάστευση μη νευρικών κυττάρων και…

Subjects/Keywords: Ανάπτυξη νευρικού συστήματος; Καθοδήγηση αξόνων; Κυτταρική μετανάστευση; Αύξηση αξόνων; Σχηματισμός δενδριτικών βρόγχων; Κυτταρική μορφογέννεση; Μόρια κυτταρικής συνάφειας; Νηματώδης; IgCAMs; Contactins; Axon growth and guidance; Branching; Tubulogenesis; Cell morphogenesis; Cell migration; Caenorhabditis elegans

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Katidou, M. (2010). Μοριακός χαρακτηρισμός του γονιδίου rig-6: ο ρόλος του στην ανάπτυξη του Caenorhabditis elegans. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/27190

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):

Katidou, M. “Μοριακός χαρακτηρισμός του γονιδίου rig-6: ο ρόλος του στην ανάπτυξη του Caenorhabditis elegans.” 2010. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed February 27, 2021. http://hdl.handle.net/10442/hedi/27190.

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

MLA Handbook (7^th Edition):

Katidou, M. “Μοριακός χαρακτηρισμός του γονιδίου rig-6: ο ρόλος του στην ανάπτυξη του Caenorhabditis elegans.” 2010. Web. 27 Feb 2021.

Vancouver:

Katidou M. Μοριακός χαρακτηρισμός του γονιδίου rig-6: ο ρόλος του στην ανάπτυξη του Caenorhabditis elegans. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/10442/hedi/27190.

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

Council of Science Editors:

Katidou M. Μοριακός χαρακτηρισμός του γονιδίου rig-6: ο ρόλος του στην ανάπτυξη του Caenorhabditis elegans. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2010. Available from: http://hdl.handle.net/10442/hedi/27190

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

21. Σγαντζής, Νικόλαος. Ανάλυση μεταμεταγραφικών δικτύων στη φυσιολογία και τον μετασχηματισμό του πνευμονικού επιθυλίου.

Degree: 2009, University of Ioannina; Πανεπιστήμιο Ιωαννίνων

URL: http://hdl.handle.net/10442/hedi/17447

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The AU-rich binding proteins - AREBPs, are major post-transcriptional regulators of gene expression and are implicated in cellular procedures that control cell cycle proliferation, apoptosis… (more)

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The AU-rich binding proteins - AREBPs, are major post-transcriptional regulators of gene expression and are implicated in cellular procedures that control cell cycle proliferation, apoptosis and differentiation. In this study, we are focusing on the in vivo biological role of the ARE-BPs, Elavl/HuR and hnRNPD/AUF1, during the development, morphogenesis and transformation of pulmonary epithelium in the lung. The complete ablation of HuR in the mice is embryonic lethal and leads to severe developmental defects. The developmental aberrations in mutant lungs start at the early stages of branching morphogenesis. Although, HuR is not implicated in the epithelial differentiation, appears to be a key coordinator of the developmental programs that control epithelial branching morphogenesis. In specific, HuR has been shown to mediate, directly or indirectly, the expression of major lung morphogenic factors such as FGF10 and BMP4, by regulating the molecular networks of reciprocal interactions among lung mesenchyme and the adjacent epithelium. Besides, this study has indicated that the lung epithelial ablation of HuR does not affect the development of the lung. However, this epithelial HuR ablation has been observed to promote the increased proliferation of broncho-alveolar stem cells (BASCs), which in turn promote the tumorigenic procedures involved in the development of lung cancer. Therefore, HuR appears to elicit a vital role in the cellular responses implicated in the transformed phenotype of the lung through its influence on the expression, by stabilizing and/or regulating the translation, of multiple target mRNAs (such as β-catenin, c-fos and top2a) that are known to be key players during lung cancer development. Furthermore, the study on the other AREBP hnRNPD/AUF1, demonstrated that the hnRNPD/AUF1 null mice although are born, show low survival rates, smaller size and sterility. Collectively, our data reveal the essential role of HuR in the cellular developmental and tumorigenic processes of the lung epithelium, whereas the AUF1 doesn’t emerge as a key competitor neither in the development nor in the pathophysiology of the lung.

Οι ριβονουκλεοπρωτεΐνες που προσδένουν mRNAs με στοιχεία πλούσια σε αδενίνη και ουρακίλη (AU-rich binding proteins - AREBPs), κατέχουν ιδιαίτερη θέση στη μετά-μεταγραφική ρύθμιση της γονιδιακής έκφρασης και εμπλέκονται σε κυτταρικές διαδικασίες που ελέγχουν τον πολλαπλασιασμό, την απόπτωση και τη διαφοροποίηση. Η παρούσα ερευνητική μελέτη αναλύει το βιολογικό ρόλο των ARE-BPs HuR και hnRNPD/AUF1 in vivo, στην ανάπτυξη, στη φυσιολογία και στο μετασχηματισμό του πνεύμονα. Για την ανάλυση αυτή, δημιουργήθηκαν καινοτόμα διαγονιδιακά συστήματα απαλοιφής της HuR και εφαρμόστηκαν πειραματικά πρότυπα καρκινογένεσης. Η καθολική απαλοιφή της HuR στον ποντικό προκαλεί σοβαρές αναπτυξιακές διαταραχές στον πνεύμονα. Συγκεκριμένα, οι αναπτυξιακές διαταραχές στον πνεύμονα των μεταλλαγμένων εμβρύων εμφανίζονται κατά τα στάδια ανάπτυξης του βρογχικού δένδρου. Σύμφωνα με τα αποτελέσματά μας, η HuR δεν…

Subjects/Keywords: Πρωτεΐνες που δεσμεύουν RNA; Μεταγραφικός έλεγχος; Μορφογένεση βρογχικού δένδρου; Πνεύμονες, Ανάπτυξη; Μετασχηματισμός πνευμονικού επιθηλίου; Βρογχοκυψελιδικά βλαστικά κύτταρα; Καρκινογένεση, Χημικά επαγόμενη; Αδενίνη, Στοιχεία πλούσια σε; Ουρακίλη, Στοιχεία πλούσια σε; RNA binding proteins; Post-transcriptional control; Lung branching morphogenesis; Lung development; Transformation of lung epithelium; Bronchioalveolar stem cells; Carcinogenesis, Chemical induced; AU rich elements - AREs

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

APA (6^th Edition):

Σγαντζής, . �. (2009). Ανάλυση μεταμεταγραφικών δικτύων στη φυσιολογία και τον μετασχηματισμό του πνευμονικού επιθυλίου. (Thesis). University of Ioannina; Πανεπιστήμιο Ιωαννίνων. Retrieved from http://hdl.handle.net/10442/hedi/17447

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):

Σγαντζής, Νικόλαος. “Ανάλυση μεταμεταγραφικών δικτύων στη φυσιολογία και τον μετασχηματισμό του πνευμονικού επιθυλίου.” 2009. Thesis, University of Ioannina; Πανεπιστήμιο Ιωαννίνων. Accessed February 27, 2021. http://hdl.handle.net/10442/hedi/17447.

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

MLA Handbook (7^th Edition):

Σγαντζής, Νικόλαος. “Ανάλυση μεταμεταγραφικών δικτύων στη φυσιολογία και τον μετασχηματισμό του πνευμονικού επιθυλίου.” 2009. Web. 27 Feb 2021.

Vancouver:

Σγαντζής �. Ανάλυση μεταμεταγραφικών δικτύων στη φυσιολογία και τον μετασχηματισμό του πνευμονικού επιθυλίου. [Internet] [Thesis]. University of Ioannina; Πανεπιστήμιο Ιωαννίνων; 2009. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/10442/hedi/17447.

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

Council of Science Editors:

Σγαντζής �. Ανάλυση μεταμεταγραφικών δικτύων στη φυσιολογία και τον μετασχηματισμό του πνευμονικού επιθυλίου. [Thesis]. University of Ioannina; Πανεπιστήμιο Ιωαννίνων; 2009. Available from: http://hdl.handle.net/10442/hedi/17447

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

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Open Access Theses and Dissertations