Morphological investigations into the development of the mammalian corneal endothelium using the mouse model

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dc.contributor.advisorKidson, Sueen_ZA
dc.contributor.authorMgwebi, Thandiswaen_ZA
dc.date.accessioned2014-07-28T18:17:30Z
dc.date.available2014-07-28T18:17:30Z
dc.date.issued2004en_ZA
dc.descriptionIncludes bibliographical references (leaves 83-89).
dc.description.abstractThe corneal endothelium (CE), a mesenchyme-derived tissue, is a monolayer of squamous cells on the inner corneal surface. In Foxc1-1• mice, the CE fails to form. The understanding of the cause of this defect has implications for the study of human eye disorders that are related to FOXC1 mutations. To understand the basis of CE defects in Foxc1-1- mice, an analysis of normal CE development was performed using scanning electron microscopy. Results showed that in normal mice the transformation from mesenchyme to endothelium was initiated at embryonic day (E) 12.5 and was characterised by a change from stellate to cobblestone shape and the formation of junctions. In FoxcN- mice, the process was initiated but a cobblestone shape not attained. The expression of adherens (N-cadherin) and tight junction (Z0-1) proteins was investigated by immunoflouresence microscopy. In the normal embryo, the expression of N-cadherin was initially in cytoplasmic vesicles and later at the cell membranes. ZO-l was first detected at the cell peripheries at E13.5. In Foxct-I- mice, N-cadherin peripheral bands failed to form. ZO-l was not expressed. These results suggest that the failure to form a monolayered CE in Foxc1 mice is due to incomplete mesenchyme-endothelial conversion. Junction formation was further investigated in vitro. N-cadherin was cytoplasmic in pre-confluent cells and at cell edges in confluent cells. ZO-l was not detected. These results suggest that in vitro, these cells are either unable to form tight junctions or the culture medium does not contain the appropriate signalling molecules.en_ZA
dc.identifier.apacitationMgwebi, T. (2004). <i>Morphological investigations into the development of the mammalian corneal endothelium using the mouse model</i>. (Thesis). University of Cape Town ,Faculty of Health Sciences ,Department of Human Biology. Retrieved from http://hdl.handle.net/11427/3268en_ZA
dc.identifier.chicagocitationMgwebi, Thandiswa. <i>"Morphological investigations into the development of the mammalian corneal endothelium using the mouse model."</i> Thesis., University of Cape Town ,Faculty of Health Sciences ,Department of Human Biology, 2004. http://hdl.handle.net/11427/3268en_ZA
dc.identifier.citationMgwebi, T. 2004. Morphological investigations into the development of the mammalian corneal endothelium using the mouse model. University of Cape Town.en_ZA
dc.identifier.ris TY - Thesis / Dissertation AU - Mgwebi, Thandiswa AB - The corneal endothelium (CE), a mesenchyme-derived tissue, is a monolayer of squamous cells on the inner corneal surface. In Foxc1-1• mice, the CE fails to form. The understanding of the cause of this defect has implications for the study of human eye disorders that are related to FOXC1 mutations. To understand the basis of CE defects in Foxc1-1- mice, an analysis of normal CE development was performed using scanning electron microscopy. Results showed that in normal mice the transformation from mesenchyme to endothelium was initiated at embryonic day (E) 12.5 and was characterised by a change from stellate to cobblestone shape and the formation of junctions. In FoxcN- mice, the process was initiated but a cobblestone shape not attained. The expression of adherens (N-cadherin) and tight junction (Z0-1) proteins was investigated by immunoflouresence microscopy. In the normal embryo, the expression of N-cadherin was initially in cytoplasmic vesicles and later at the cell membranes. ZO-l was first detected at the cell peripheries at E13.5. In Foxct-I- mice, N-cadherin peripheral bands failed to form. ZO-l was not expressed. These results suggest that the failure to form a monolayered CE in Foxc1 mice is due to incomplete mesenchyme-endothelial conversion. Junction formation was further investigated in vitro. N-cadherin was cytoplasmic in pre-confluent cells and at cell edges in confluent cells. ZO-l was not detected. These results suggest that in vitro, these cells are either unable to form tight junctions or the culture medium does not contain the appropriate signalling molecules. DA - 2004 DB - OpenUCT DP - University of Cape Town LK - https://open.uct.ac.za PB - University of Cape Town PY - 2004 T1 - Morphological investigations into the development of the mammalian corneal endothelium using the mouse model TI - Morphological investigations into the development of the mammalian corneal endothelium using the mouse model UR - http://hdl.handle.net/11427/3268 ER - en_ZA
dc.identifier.urihttp://hdl.handle.net/11427/3268
dc.identifier.vancouvercitationMgwebi T. Morphological investigations into the development of the mammalian corneal endothelium using the mouse model. [Thesis]. University of Cape Town ,Faculty of Health Sciences ,Department of Human Biology, 2004 [cited yyyy month dd]. Available from: http://hdl.handle.net/11427/3268en_ZA
dc.language.isoengen_ZA
dc.publisher.departmentDepartment of Human Biologyen_ZA
dc.publisher.facultyFaculty of Health Sciencesen_ZA
dc.publisher.institutionUniversity of Cape Town
dc.subject.otherMedicineen_ZA
dc.titleMorphological investigations into the development of the mammalian corneal endothelium using the mouse modelen_ZA
dc.typeDoctoral Thesis
dc.type.qualificationlevelDoctoral
dc.type.qualificationnamePhDen_ZA
uct.type.filetypeText
uct.type.filetypeImage
uct.type.publicationResearchen_ZA
uct.type.resourceThesisen_ZA
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