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10.1152/ajprenal.00196.2016 http://scihub22266oqcxt.onion/10.1152/ajprenal.00196.2016 C5142165!5142165 !27440779     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27440779 &cmd=llinks): Failed to open stream: HTTP request failed! 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Reducing mTOR augments parietal epithelial cell density in a model of acute podocyte depletion and in aged kidneys |pdf=|usr=}}{{27440779 }} gab.com Text Reducing mTOR augments parietal epithelial cell density in a model of acute podocyte depletion and in aged kidneys JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27440779 #FOAvip Parietal epithelial cell (PEC) response to glomerular injury may underlie a common pathway driving fibrogenesis following podocyte loss that typifies several glomerular disorders. Although the mammalian target of rapamycin (mTOR) pathway is important in cell homeostasis, little is known of the biological role or impact of reducing mTOR activity on PEC response following podocyte depletion, nor in the aging kidney. The purpose of these studies was to determine the impact on PECs of reducing mTOR activity following abrupt experimental depletion in podocyte number, as well as in a model of chronic podocyte loss and sclerosis associated with aging. Podocyte depletion was induced by an anti-podocyte antibody and rapamycin started at day 5 until death at day 14 Reducing mTOR did not lead to a greater reduction in podocyte density, despite greater glomerulosclerosis. However, mTOR inhibition lead to an increase in PEC density and PEC-derived crescent formation. Additionally, markers of epithelial-to-mesenchymal transition (platelet-derived growth factor receptor-?, ?-smooth muscle actin, Notch-3) and PEC activation (CD44, collagen IV) were further increased by mTOR reduction. Aged mice treated with rapamycin for 1, 2, and 10 wk before death at 26.5 mo (?75-yr-old human age) had increased the number of glomeruli with a crescentic appearance. mTOR inhibition at either a high or low level lead to changes in PEC phenotype, indicating PEC morphology is sensitive to changes mediated by global mTOR inhibition. Twit Text FOAVip Reducing mTOR augments parietal epithelial cell density in a model of acute podocyte depletion and in aged kidneys ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27440779 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27440779 #FOAvip English Wikipedia <ref>{{Cite pmid|27440779 }}</ref> Reducing mTOR augments parietal epithelial cell density in a model of acute podocyte depletion and in aged kidneys #MMPMID27440779 McNicholas BA ; Eng DG ; Lichtnekert J ; Rabinowitz PS ; Pippin JW ; Shankland SJ Am J Physiol Renal Physiol 2016[Sep]; 311 (3 ): F626-39 PMID27440779 show ga Parietal epithelial cell (PEC) response to glomerular injury may underlie a common pathway driving fibrogenesis following podocyte loss that typifies several glomerular disorders. Although the mammalian target of rapamycin (mTOR) pathway is important in cell homeostasis, little is known of the biological role or impact of reducing mTOR activity on PEC response following podocyte depletion, nor in the aging kidney. The purpose of these studies was to determine the impact on PECs of reducing mTOR activity following abrupt experimental depletion in podocyte number, as well as in a model of chronic podocyte loss and sclerosis associated with aging. Podocyte depletion was induced by an anti-podocyte antibody and rapamycin started at day 5 until death at day 14 Reducing mTOR did not lead to a greater reduction in podocyte density, despite greater glomerulosclerosis. However, mTOR inhibition lead to an increase in PEC density and PEC-derived crescent formation. Additionally, markers of epithelial-to-mesenchymal transition (platelet-derived growth factor receptor-?, ?-smooth muscle actin, Notch-3) and PEC activation (CD44, collagen IV) were further increased by mTOR reduction. Aged mice treated with rapamycin for 1, 2, and 10 wk before death at 26.5 mo (?75-yr-old human age) had increased the number of glomeruli with a crescentic appearance. mTOR inhibition at either a high or low level lead to changes in PEC phenotype, indicating PEC morphology is sensitive to changes mediated by global mTOR inhibition. |Aging/*metabolism/pathology [MESH] |Animals [MESH] |Cell Count [MESH] |Epithelial Cells/drug effects/*metabolism/pathology [MESH] |Epithelial-Mesenchymal Transition [MESH] |Female [MESH] |Glomerulosclerosis, Focal Segmental/*metabolism/pathology [MESH] |Kidney Glomerulus/drug effects/metabolism/pathology [MESH] |Kidney/drug effects/*metabolism/pathology [MESH] |Male [MESH] |Mice [MESH] |Podocytes/drug effects/*metabolism/pathology [MESH] |Sirolimus/pharmacology [MESH]Reducing mTOR augments parietal epithelial cell density in a model of (epmc).pdf DeepDyve Pubget Overpricing