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10.1186/s13069-015-0022-0 http://scihub22266oqcxt.onion/10.1186/s13069-015-0022-0 C4379608!4379608 !25829947     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 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\25829947 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Fibrogenesis+Tissue+Repair 2015 ; 8 (ä): 5 Nephropedia Template TP {{tp|p=25829947 |t=2015. Human lung myofibroblast TGF?1-dependent Smad2/3 signalling is Ca(2+)-dependent and regulated by KCa3 1 K(+) channels |pdf=|usr=}}{{25829947 }} gab.com Text Human lung myofibroblast TGF 1-dependent Smad2/3 signalling is Ca(2+)-dependent and regulated by KCa3 1 K(+) channels JO: Fibrogenesis Tissue Repair http://www.kidney.de/pget.php?&tw=1&pmid=25829947 #FOAvip BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a common and invariably lethal interstitial lung disease with poorly effective therapy. Blockade of the K(+) channel KCa3.1 reduces constitutive ?-SMA and Smad2/3 nuclear translocation in IPF-derived human lung myofibroblasts (HLMFs), and inhibits several transforming growth factor beta 1 (TGF?1)-dependent cell processes. We hypothesized that KCa3.1-dependent cell processes also regulate the TGF?1-dependent Smad2/3 signalling pathway in HLMFs. HLMFs obtained from non-fibrotic controls (NFC) and IPF lungs were grown in vitro and examined for ?SMA expression by immunofluorescence, RT-PCR, and flow cytometry. Two specific and distinct KCa3.1 blockers (TRAM-34 200 nM and ICA-17043 [Senicapoc] 100 nM) were used to determine their effects on TGF?1-dependent signalling. Expression of phosphorylated and total Smad2/3 following TGF?1 stimulation was determined by Western blot and Smad2/3 nuclear translocation by immunofluorescence. RESULTS: KCa3.1 block attenuated TGF?1-dependent Smad2/3 phosphorylation and nuclear translocation, and this was mimicked by lowering the extracellular Ca(2+) concentration. KCa3.1 block also inhibited Smad2/3-dependent gene transcription (?SMA, collagen type I), inhibited KCa3.1 mRNA expression, and attenuated TGF?1-dependent ?SMA protein expression. CONCLUSIONS: KCa3.1 activity regulates TGF?1-dependent effects in NFC- and IPF-derived primary HLMFs through the regulation of the TGF?1/Smad signalling pathway, with promotion of downstream gene transcription and protein expression. KCa3.1 blockers may offer a novel approach to treating IPF. Twit Text FOAVip Human lung myofibroblast TGF 1-dependent Smad2/3 signalling is Ca(2+)-dependent and regulated by KCa3 1 K(+) channels ????Fibrogenesis Tissue Repair http://www.kidney.de/pget.php?&tw=1&pmid=25829947 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25829947 #FOAvip English Wikipedia <ref>{{Cite pmid|25829947 }}</ref> Human lung myofibroblast TGF?1-dependent Smad2/3 signalling is Ca(2+)-dependent and regulated by KCa3 1 K(+) channels #MMPMID25829947 Roach KM ; Feghali-Bostwick C ; Wulff H ; Amrani Y ; Bradding P Fibrogenesis Tissue Repair 2015[]; 8 (ä): 5 PMID25829947 show ga BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a common and invariably lethal interstitial lung disease with poorly effective therapy. Blockade of the K(+) channel KCa3.1 reduces constitutive ?-SMA and Smad2/3 nuclear translocation in IPF-derived human lung myofibroblasts (HLMFs), and inhibits several transforming growth factor beta 1 (TGF?1)-dependent cell processes. We hypothesized that KCa3.1-dependent cell processes also regulate the TGF?1-dependent Smad2/3 signalling pathway in HLMFs. HLMFs obtained from non-fibrotic controls (NFC) and IPF lungs were grown in vitro and examined for ?SMA expression by immunofluorescence, RT-PCR, and flow cytometry. Two specific and distinct KCa3.1 blockers (TRAM-34 200 nM and ICA-17043 [Senicapoc] 100 nM) were used to determine their effects on TGF?1-dependent signalling. Expression of phosphorylated and total Smad2/3 following TGF?1 stimulation was determined by Western blot and Smad2/3 nuclear translocation by immunofluorescence. RESULTS: KCa3.1 block attenuated TGF?1-dependent Smad2/3 phosphorylation and nuclear translocation, and this was mimicked by lowering the extracellular Ca(2+) concentration. KCa3.1 block also inhibited Smad2/3-dependent gene transcription (?SMA, collagen type I), inhibited KCa3.1 mRNA expression, and attenuated TGF?1-dependent ?SMA protein expression. CONCLUSIONS: KCa3.1 activity regulates TGF?1-dependent effects in NFC- and IPF-derived primary HLMFs through the regulation of the TGF?1/Smad signalling pathway, with promotion of downstream gene transcription and protein expression. KCa3.1 blockers may offer a novel approach to treating IPF. äHuman lung myofibroblast TGF?1-dependent Smad2/3 signalling is Ca(2+)-(epmc).pdf DeepDyve Pubget Overpricing