BIGH3 dependent renal cell apoptosis and the role of macrophage-derived TGFbeta1

dc.contributor.advisorLeBaron, Richard G.
dc.contributor.authorMoritz, Robert Joseph
dc.contributor.committeeMemberTsin, Andrew T.
dc.contributor.committeeMemberPhelix, Clyde
dc.date.accessioned2024-02-12T18:29:13Z
dc.date.available2024-02-12T18:29:13Z
dc.date.issued2012
dc.descriptionThis item is available only to currently enrolled UTSA students, faculty or staff. To download, navigate to Log In in the top right-hand corner of this screen, then select Log in with my UTSA ID.
dc.description.abstractDiabetes mellitus associated renal damage is characterized by the recruitment of macrophages to the renal cortex and an accumulation of extracellular cellular matrix (ECM) molecules. Transforming Growth Factor Beta- Induced Gene Human Clone 3 (BIGH3) is a secreted, pro-apoptotic ECM molecule distinguished by an increased rate of synthesis in many cells stimulated with Transforming growth factor beta (TGFbeta). Macrophages have been shown to be a source of secreted TGFbeta1, and BIGH3 levels are found to be elevated in the diabetic kidney. Our previous studies have detected an increased synthesis of BIGH3 in response to TGFbeta1 in the kidney, eye and vasculature of mice and human cells in culture. These studies have also detected an increase in levels of detected apoptosis of kidney and eye cells cultured in an accumulation of BIGH3. This study further pursues these findings by demonstrating a dose-dependent apoptotic response in human renal proximal tubule epithelial cells (RPTEC). Additionally, we attenuated an apoptotic response in RPTEC cultured in medium enriched with macrophage-derived factors through the use of antibodies and agents which neutralize elements of the TGFbeta1 signaling pathway. The dynamics of these responses are explored by comparing rates of BIGH3 mRNA expression and quantified levels of apoptosis in RPTEC stimulated with factors derived from macrophages cultured under normal and diabetic conditions. These data explore a mechanistic relationship between TGFbeta1 derived from macrophages in a diabetic environment, the expression and accumulation of BIGH3, and induced apoptosis in renal cells.
dc.description.departmentIntegrative Biology
dc.format.extent45 pages
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12588/4781
dc.languageen
dc.subjectapoptosis
dc.subjectBIGH3
dc.subjectRenal
dc.subjectTGFB1
dc.subject.classificationBiology
dc.subject.classificationMolecular biology
dc.subject.classificationCellular biology
dc.titleBIGH3 dependent renal cell apoptosis and the role of macrophage-derived TGFbeta1
dc.typeThesis
dc.type.dcmiText
dcterms.accessRightspq_closed
thesis.degree.departmentIntegrative Biology
thesis.degree.grantorUniversity of Texas at San Antonio
thesis.degree.levelMasters
thesis.degree.nameMaster of Science

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