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10.1111/jcmm.13526 http://scihub22266oqcxt.onion/10.1111/jcmm.13526 C5867168!5867168!29424488     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Mol+Med 2018 ; 22 (4): 2346-56 Nephropedia Template TP {{tp|p=29424488|t=2018. Lipopolysaccharide enhances TGF??1 signalling pathway and rat pancreatic fibrosis |pdf=|usr=}}{{29424488}} gab.com Text Lipopolysaccharide enhances TGF 1 signalling pathway and rat pancreatic fibrosis JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29424488 #FOAvip Pancreatic stellate cells (PSCs) play a critical role in fibrogenesis during alcoholic chronic pancreatitis (ACP). Transforming growth factor?beta1 (TGF??1) is a key regulator of extracellular matrix production and PSC activation. Endotoxin lipopolysaccharide (LPS) has been recognized as a trigger factor in the pathogenesis of ACP. This study aimed to investigate the mechanisms by which LPS modulates TGF??1 signalling and pancreatic fibrosis. Sprague?Dawley rats fed with a Lieber?DeCarli alcohol (ALC) liquid diet for 10 weeks with or without LPS challenge during the last 3 weeks. In vitro studies were performed using rat macrophages (M?s) and PSCs (RP?2 cell line). The results showed that repeated LPS challenge resulted in significantly more collagen production and PSC activation compared to rats fed with ALC alone. LPS administration caused overexpression of pancreatic TLR4 or TGF??1 which was paralleled by an increased number of TLR4?positive or TGF??1?positive M?s or PSCs in ALC?fed rats. In vitro, TLR4 or TGF??1 production in M?s or RP?2 cells was up?regulated by LPS. LPS alone or in combination with TGF??1 significantly increased type I collagen and ??SMA production and Smad2 and 3 phosphorylation in serum?starved RP?2 cells. TGF?? pseudoreceptor BAMBI production was repressed by LPS, which was antagonized by Si?TLR4 RNA or by inhibitors of MyD88/NF?kB. Additionally, knockdown of Bambi with Si?Bambi RNA significantly increased TGF??1 signalling in RP?2 cells. These findings indicate that LPS increases TGF??1 production through paracrine and autocrine mechanisms and that LPS enhances TGF??1 signalling in PSCs by repressing BAMBI via TLR4/MyD88/NF?kB activation. Twit Text FOAVip Lipopolysaccharide enhances TGF 1 signalling pathway and rat pancreatic fibrosis ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=29424488 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29424488 #FOAvip English Wikipedia <ref>{{Cite pmid|29424488}}</ref> Lipopolysaccharide enhances TGF??1 signalling pathway and rat pancreatic fibrosis #MMPMID29424488 Sun L; Xiu M; Wang S; Brigstock DR; Li H; Qu L; Gao R J Cell Mol Med 2018[Apr]; 22 (4): 2346-56 PMID29424488show ga Pancreatic stellate cells (PSCs) play a critical role in fibrogenesis during alcoholic chronic pancreatitis (ACP). Transforming growth factor?beta1 (TGF??1) is a key regulator of extracellular matrix production and PSC activation. Endotoxin lipopolysaccharide (LPS) has been recognized as a trigger factor in the pathogenesis of ACP. This study aimed to investigate the mechanisms by which LPS modulates TGF??1 signalling and pancreatic fibrosis. Sprague?Dawley rats fed with a Lieber?DeCarli alcohol (ALC) liquid diet for 10 weeks with or without LPS challenge during the last 3 weeks. In vitro studies were performed using rat macrophages (M?s) and PSCs (RP?2 cell line). The results showed that repeated LPS challenge resulted in significantly more collagen production and PSC activation compared to rats fed with ALC alone. LPS administration caused overexpression of pancreatic TLR4 or TGF??1 which was paralleled by an increased number of TLR4?positive or TGF??1?positive M?s or PSCs in ALC?fed rats. In vitro, TLR4 or TGF??1 production in M?s or RP?2 cells was up?regulated by LPS. LPS alone or in combination with TGF??1 significantly increased type I collagen and ??SMA production and Smad2 and 3 phosphorylation in serum?starved RP?2 cells. TGF?? pseudoreceptor BAMBI production was repressed by LPS, which was antagonized by Si?TLR4 RNA or by inhibitors of MyD88/NF?kB. Additionally, knockdown of Bambi with Si?Bambi RNA significantly increased TGF??1 signalling in RP?2 cells. These findings indicate that LPS increases TGF??1 production through paracrine and autocrine mechanisms and that LPS enhances TGF??1 signalling in PSCs by repressing BAMBI via TLR4/MyD88/NF?kB activation. äLipopolysaccharide enhances TGF??1 signalling pathway and rat pancreat(epmc).pdf DeepDyve Pubget Overpricing