Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1242/dmm.020511 http://scihub22266oqcxt.onion/10.1242/dmm.020511 C4527294!4527294!26092126     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Dis+Model+Mech 2015 ; 8 (8): 931-40 Nephropedia Template TP {{tp|p=26092126|t=2015. Glycogen synthase kinase-3 inhibition attenuates fibroblast activation and development of fibrosis following renal ischemia-reperfusion in mice |pdf=|usr=}}{{26092126}} gab.com Text Glycogen synthase kinase-3 inhibition attenuates fibroblast activation and development of fibrosis following renal ischemia-reperfusion in mice JO: Dis Model Mech http://www.kidney.de/pget.php?&tw=1&pmid=26092126 #FOAvip Glycogen synthase kinase-3? (GSK3?) is a serine/threonine protein kinase that plays an important role in renal tubular injury and regeneration in acute kidney injury. However, its role in the development of renal fibrosis, often a long-term consequence of acute kidney injury, is unknown. Using a mouse model of renal fibrosis induced by ischemia-reperfusion injury, we demonstrate increased GSK3? expression and activity in fibrotic kidneys, and its presence in myofibroblasts in addition to tubular epithelial cells. Pharmacological inhibition of GSK3 using TDZD-8 starting before or after ischemia-reperfusion significantly suppressed renal fibrosis by reducing the myofibroblast population, collagen-1 and fibronectin deposition, inflammatory cytokines, and macrophage infiltration. GSK3 inhibition in vivo reduced TGF-?1, SMAD3 activation and plasminogen activator inhibitor-1 levels. Consistently in vitro, TGF-?1 treatment increased GSK3? expression and GSK3 inhibition abolished TGF-?1-induced SMAD3 activation and ?-smooth muscle actin (?-SMA) expression in cultured renal fibroblasts. Importantly, overexpression of constitutively active GSK3? stimulated ?-SMA expression even in the absence of TGF-?1 treatment. These results suggest that TGF-? regulates GSK3?, which in turn is important for TGF-??SMAD3 signaling and fibroblast-to-myofibroblast differentiation. Overall, these studies demonstrate that GSK3 could promote renal fibrosis by activation of TGF-? signaling and the use of GSK3 inhibitors might represent a novel therapeutic approach for progressive renal fibrosis that develops as a consequence of acute kidney injury. Twit Text FOAVip Glycogen synthase kinase-3 inhibition attenuates fibroblast activation and development of fibrosis following renal ischemia-reperfusion in mice ????Dis Model Mech http://www.kidney.de/pget.php?&tw=1&pmid=26092126 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26092126 #FOAvip English Wikipedia <ref>{{Cite pmid|26092126}}</ref> Glycogen synthase kinase-3 inhibition attenuates fibroblast activation and development of fibrosis following renal ischemia-reperfusion in mice #MMPMID26092126 Singh SP; Tao S; Fields TA; Webb S; Harris RC; Rao R Dis Model Mech 2015[Aug]; 8 (8): 931-40 PMID26092126show ga Glycogen synthase kinase-3? (GSK3?) is a serine/threonine protein kinase that plays an important role in renal tubular injury and regeneration in acute kidney injury. However, its role in the development of renal fibrosis, often a long-term consequence of acute kidney injury, is unknown. Using a mouse model of renal fibrosis induced by ischemia-reperfusion injury, we demonstrate increased GSK3? expression and activity in fibrotic kidneys, and its presence in myofibroblasts in addition to tubular epithelial cells. Pharmacological inhibition of GSK3 using TDZD-8 starting before or after ischemia-reperfusion significantly suppressed renal fibrosis by reducing the myofibroblast population, collagen-1 and fibronectin deposition, inflammatory cytokines, and macrophage infiltration. GSK3 inhibition in vivo reduced TGF-?1, SMAD3 activation and plasminogen activator inhibitor-1 levels. Consistently in vitro, TGF-?1 treatment increased GSK3? expression and GSK3 inhibition abolished TGF-?1-induced SMAD3 activation and ?-smooth muscle actin (?-SMA) expression in cultured renal fibroblasts. Importantly, overexpression of constitutively active GSK3? stimulated ?-SMA expression even in the absence of TGF-?1 treatment. These results suggest that TGF-? regulates GSK3?, which in turn is important for TGF-??SMAD3 signaling and fibroblast-to-myofibroblast differentiation. Overall, these studies demonstrate that GSK3 could promote renal fibrosis by activation of TGF-? signaling and the use of GSK3 inhibitors might represent a novel therapeutic approach for progressive renal fibrosis that develops as a consequence of acute kidney injury. äGlycogen synthase kinase-3 inhibition attenuates fibroblast activation(epmc).pdf DeepDyve Pubget Overpricing