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10.1111/jnc.12710 http://scihub22266oqcxt.onion/10.1111/jnc.12710 C4065629!4065629!24606313     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 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       J+Neurochem 2014 ; 130 (1): 41-9 Nephropedia Template TP {{tp|p=24606313|t=2014. Targeted inhibition of KCa3 1 attenuates TGF-?-induced reactive astrogliosis through the Smad2/3 signaling pathway |pdf=|usr=}}{{24606313}} gab.com Text Targeted inhibition of KCa3 1 attenuates TGF- -induced reactive astrogliosis through the Smad2/3 signaling pathway JO: J Neurochem http://www.kidney.de/pget.php?&tw=1&pmid=24606313 #FOAvip Reactive astrogliosis, characterized by cellular hypertrophy and various alterations in gene expressionand proliferative phenotypes, is considered to contribute to brain injuries and diseases as diverse as trauma, neurodegeneration, and ischemia. KCa3.1, a potassium channel protein, has been reported to be up-regulated in reactive astrocytes after spinal cord injury in vivo. However, little is known regarding the exact role of KCa3.1 in reactive astrogliosis. To elucidate the role of KCa3.1 in regulating reactive astrogliosis, we investigated the effects of either blocking or knockout of KCa3.1 channels on the production of astrogliosis and astrocytic proliferation in response to transforming growth factor (TGF)-? in primary cultures of mouse astrocytes. We found that TGF-? increased KCa3.1 protein expression in astrocytes, with a concomitant marked increase in the expression of reactive astrogliosis, including glial fibrillary acidic protein (GFAP) and chondroitin sulfate proteoglycans (CSPGs). These changes were significantly attenuated by the KCa3.1 inhibitor TRAM-34. Similarly, the increase in GFAP and CSPGs in response to TGF-? was attenuated in KCa3.1?/? astrocytes. TRAM-34 also suppressed astrocytic proliferation. Additionally, the TGF-?-induced phosphorylation of Smad2 and Smad3 proteins was reduced with either inhibition of KCa3.1 with TRAM-34 or in KCa3.1?/? astrocytes. These findings highlight a novel role for the KCa3.1 channel in reactive astrogliosis phenotypic modulation and provide a potential target for therapeutic intervention for brain injuries. Twit Text FOAVip Targeted inhibition of KCa3 1 attenuates TGF- -induced reactive astrogliosis through the Smad2/3 signaling pathway ????J Neurochem http://www.kidney.de/pget.php?&tw=1&pmid=24606313 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24606313 #FOAvip English Wikipedia <ref>{{Cite pmid|24606313}}</ref> Targeted inhibition of KCa3 1 attenuates TGF-?-induced reactive astrogliosis through the Smad2/3 signaling pathway #MMPMID24606313 Yu Z; Yu P; Chen H; Geller HM J Neurochem 2014[Jul]; 130 (1): 41-9 PMID24606313show ga Reactive astrogliosis, characterized by cellular hypertrophy and various alterations in gene expressionand proliferative phenotypes, is considered to contribute to brain injuries and diseases as diverse as trauma, neurodegeneration, and ischemia. KCa3.1, a potassium channel protein, has been reported to be up-regulated in reactive astrocytes after spinal cord injury in vivo. However, little is known regarding the exact role of KCa3.1 in reactive astrogliosis. To elucidate the role of KCa3.1 in regulating reactive astrogliosis, we investigated the effects of either blocking or knockout of KCa3.1 channels on the production of astrogliosis and astrocytic proliferation in response to transforming growth factor (TGF)-? in primary cultures of mouse astrocytes. We found that TGF-? increased KCa3.1 protein expression in astrocytes, with a concomitant marked increase in the expression of reactive astrogliosis, including glial fibrillary acidic protein (GFAP) and chondroitin sulfate proteoglycans (CSPGs). These changes were significantly attenuated by the KCa3.1 inhibitor TRAM-34. Similarly, the increase in GFAP and CSPGs in response to TGF-? was attenuated in KCa3.1?/? astrocytes. TRAM-34 also suppressed astrocytic proliferation. Additionally, the TGF-?-induced phosphorylation of Smad2 and Smad3 proteins was reduced with either inhibition of KCa3.1 with TRAM-34 or in KCa3.1?/? astrocytes. These findings highlight a novel role for the KCa3.1 channel in reactive astrogliosis phenotypic modulation and provide a potential target for therapeutic intervention for brain injuries. äTargeted inhibition of KCa3 1 attenuates TGF-?-induced reactive astrog(epmc).pdf DeepDyve Pubget Overpricing