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10.1152/ajplung.00333.2007 http://scihub22266oqcxt.onion/10.1152/ajplung.00333.2007 C5926773!5926773!18162602     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Lung+Cell+Mol+Physiol 2008 ; 294 (5): L891-901 Nephropedia Template TP {{tp|p=18162602|t=2008. PPAR-? agonists inhibit profibrotic phenotypes in human lung fibroblasts and bleomycin-induced pulmonary fibrosis |pdf=|usr=}}{{18162602}} gab.com Text PPAR- agonists inhibit profibrotic phenotypes in human lung fibroblasts and bleomycin-induced pulmonary fibrosis JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=18162602 #FOAvip Pulmonary fibrosis is characterized by alterations in fibroblast phenotypes resulting in excessive extracellular matrix accumulation and anatomic remodeling. Current therapies for this condition are largely ineffective. Peroxisome proliferator-activated receptor-? (PPAR-?) is a member of the nuclear hormone receptor superfamily, the activation of which produces a number of biological effects, including alterations in metabolic and inflammatory responses. The role of PPAR-? as a potential therapeutic target for fibrotic lung diseases remains undefined. In the present study, we show expression of PPAR-? in fibroblasts obtained from normal human lungs and lungs of patients with idiopathic interstitial pneumonias. Treatment of lung fibroblasts and myofibroblasts with PPAR-? agonists results in inhibition of proliferative responses and induces cell cycle arrest. In addition, PPAR-? agonists, including a constitutively active PPAR-? construct (VP16-PPAR-?), inhibit the ability of transforming growth factor-?1 to induce myofibroblast differentiation and collagen secretion. PPAR-? agonists also inhibit fibrosis in a murine model, even when administration is delayed until after the initial inflammation has largely resolved. These observations indicate that PPAR-? is an important regulator of fibroblast/myofibroblast activation and suggest a role for PPAR-? ligands as novel therapeutic agents for fibrotic lung diseases. Twit Text FOAVip PPAR- agonists inhibit profibrotic phenotypes in human lung fibroblasts and bleomycin-induced pulmonary fibrosis ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=18162602 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18162602 #FOAvip English Wikipedia <ref>{{Cite pmid|18162602}}</ref> PPAR-? agonists inhibit profibrotic phenotypes in human lung fibroblasts and bleomycin-induced pulmonary fibrosis #MMPMID18162602 Milam JE; Keshamouni VG; Phan SH; Hu B; Gangireddy SR; Hogaboam CM; Standiford TJ; Thannickal VJ; Reddy RC Am J Physiol Lung Cell Mol Physiol 2008[May]; 294 (5): L891-901 PMID18162602show ga Pulmonary fibrosis is characterized by alterations in fibroblast phenotypes resulting in excessive extracellular matrix accumulation and anatomic remodeling. Current therapies for this condition are largely ineffective. Peroxisome proliferator-activated receptor-? (PPAR-?) is a member of the nuclear hormone receptor superfamily, the activation of which produces a number of biological effects, including alterations in metabolic and inflammatory responses. The role of PPAR-? as a potential therapeutic target for fibrotic lung diseases remains undefined. In the present study, we show expression of PPAR-? in fibroblasts obtained from normal human lungs and lungs of patients with idiopathic interstitial pneumonias. Treatment of lung fibroblasts and myofibroblasts with PPAR-? agonists results in inhibition of proliferative responses and induces cell cycle arrest. In addition, PPAR-? agonists, including a constitutively active PPAR-? construct (VP16-PPAR-?), inhibit the ability of transforming growth factor-?1 to induce myofibroblast differentiation and collagen secretion. PPAR-? agonists also inhibit fibrosis in a murine model, even when administration is delayed until after the initial inflammation has largely resolved. These observations indicate that PPAR-? is an important regulator of fibroblast/myofibroblast activation and suggest a role for PPAR-? ligands as novel therapeutic agents for fibrotic lung diseases. äPPAR-? agonists inhibit profibrotic phenotypes in human lung fibroblas(epmc).pdf DeepDyve Pubget Overpricing