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Retinoids Augment the Expression of Podocyte Proteins by Glomerular Parietal Epithelial Cells in Experimental Glomerular Disease
Author(s) -
Jiong Zhang,
Jeffrey W. Pippin,
Michael R. Vaughan,
Ronald D. Krofft,
Yoshinori Taniguchi,
Paola Romagnani,
Peter J. Nelson,
Zhihong Liu,
Stuart J. Shankland
Publication year - 2012
Publication title -
nephron experimental nephrology
Language(s) - English
Resource type - Journals
ISSN - 1660-2129
DOI - 10.1159/000342808
Subject(s) - podocyte , membranous nephropathy , glomerulosclerosis , focal segmental glomerulosclerosis , glomerulonephritis , kidney , biology , pathology , minimal change disease , synaptopodin , nephropathy , podocalyxin , endocrinology , medicine , proteinuria , diabetes mellitus
A decrease in glomerular podocyte number in membranous nephropathy and focal segmental glomerulosclerosis (FSGS) ultimately underlines glomerulosclerosis and the decrease in kidney function. Recent studies have shown that in these diseases, glomerular parietal epithelial cells begin to express proteins considered unique to podocytes, and that these glomerular epithelial transition cells might serve as podocyte progenitors. Because retinoids improve many forms of experimental glomerular disease characterized by podocyte injury and loss, we asked if all-trans retinoic acid (ATRA) induces parietal epithelial cells to express podocyte proteins.

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