Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633444
Title: Alterations in podocyte phenotype in health and disease
Author: May, Carl James
Awarding Body: University of Bristol
Current Institution: University of Bristol
Date of Award: 2013
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Abstract:
The glomerulus is the site of ultrafiltration within in the nephron of the kidney. The Glomerular Filtration Barrier (GFB) restricts protein loss whilst allowing the passage of water and small solutes. There are two cell types that contribute to the formation of the GFB: the Glomerular Endothelial Cell (GEne) and the podocyte. Both cell types contribute to the formation of the Glomerular Basement Membrane (GBM). The podocytes are composed of three structurally distinct segments: the cell body, major processes and foot processes. The foot processes regularly interdigitate. The gap between interdigitating foot processes is bridged by the slit diaphragm. The slit diaphragm is a molecular sieve that enables the podocyte to restrict urinary protein loss. Podocyte injury leads to foot process effacement 'and the concomitant loss of the slit diaphragm. Therefore podocyte injury compromises the integrity of the GFB leading to the proteinuria and nephrotic syndrome. Foot process effacement requires increased podocyte motility. Indeed, podocyte motility in vitro is being increasingly used as a marker of foot process effacement in vivo. Whilst the pathogenesis of nephrotic syndrome is not completely understood, it is well established that the podocyte is the target cell. In this study, two sources of podocyte injury have been studied.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.633444  DOI: Not available
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