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10.1016/j.kint.2016.06.032 http://scihub22266oqcxt.onion/10.1016/j.kint.2016.06.032 C5073078!5073078 !27575556     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27575556 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Kidney+Int 2016 ; 90 (5 ): 1056-1070 Nephropedia Template TP {{tp|p=27575556 |t=2016. Loss of endogenous thymosin ?(4) accelerates glomerular disease |pdf=|usr=}}{{27575556 }} gab.com Text Loss of endogenous thymosin (4) accelerates glomerular disease JO: Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=27575556 #FOAvip Glomerular disease is characterized by morphologic changes in podocyte cells accompanied by inflammation and fibrosis. Thymosin ?(4) regulates cell morphology, inflammation, and fibrosis in several organs and administration of exogenous thymosin ?(4) improves animal models of unilateral ureteral obstruction and diabetic nephropathy. However, the role of endogenous thymosin ?(4) in the kidney is unknown. We demonstrate that thymosin ?(4) is expressed prominently in podocytes of developing and adult mouse glomeruli. Global loss of thymosin ?(4) did not affect healthy glomeruli, but accelerated the severity of immune-mediated nephrotoxic nephritis with worse renal function, periglomerular inflammation, and fibrosis. Lack of thymosin ?(4) in nephrotoxic nephritis led to the redistribution of podocytes from the glomerular tuft toward the Bowman capsule suggesting a role for thymosin ?(4) in the migration of these cells. Thymosin ?(4) knockdown in cultured podocytes also increased migration in a wound-healing assay, accompanied by F-actin rearrangement and increased RhoA activity. We propose that endogenous thymosin ?(4) is a modifier of glomerular injury, likely having a protective role acting as a brake to slow disease progression. Twit Text FOAVip Loss of endogenous thymosin (4) accelerates glomerular disease ????Kidney Int http://www.kidney.de/pget.php?&tw=1&pmid=27575556 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27575556 #FOAvip English Wikipedia <ref>{{Cite pmid|27575556 }}</ref> Loss of endogenous thymosin ?(4) accelerates glomerular disease #MMPMID27575556 Vasilopoulou E ; Kolatsi-Joannou M ; Lindenmeyer MT ; White KE ; Robson MG ; Cohen CD ; Sebire NJ ; Riley PR ; Winyard PJ ; Long DA Kidney Int 2016[Nov]; 90 (5 ): 1056-1070 PMID27575556 show ga Glomerular disease is characterized by morphologic changes in podocyte cells accompanied by inflammation and fibrosis. Thymosin ?(4) regulates cell morphology, inflammation, and fibrosis in several organs and administration of exogenous thymosin ?(4) improves animal models of unilateral ureteral obstruction and diabetic nephropathy. However, the role of endogenous thymosin ?(4) in the kidney is unknown. We demonstrate that thymosin ?(4) is expressed prominently in podocytes of developing and adult mouse glomeruli. Global loss of thymosin ?(4) did not affect healthy glomeruli, but accelerated the severity of immune-mediated nephrotoxic nephritis with worse renal function, periglomerular inflammation, and fibrosis. Lack of thymosin ?(4) in nephrotoxic nephritis led to the redistribution of podocytes from the glomerular tuft toward the Bowman capsule suggesting a role for thymosin ?(4) in the migration of these cells. Thymosin ?(4) knockdown in cultured podocytes also increased migration in a wound-healing assay, accompanied by F-actin rearrangement and increased RhoA activity. We propose that endogenous thymosin ?(4) is a modifier of glomerular injury, likely having a protective role acting as a brake to slow disease progression. |Animals [MESH] |Cell Movement [MESH] |Cells, Cultured [MESH] |Cytoskeleton/metabolism [MESH] |Fibrosis [MESH] |Glomerulonephritis/*metabolism/pathology [MESH] |Kidney Glomerulus/pathology [MESH] |Macrophages [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Podocytes/*metabolism [MESH]Loss of endogenous thymosin ?(4) accelerates glomerular disease (epmc).pdf DeepDyve Pubget Overpricing