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10.1152/ajplung.00333.2007 http://scihub22266oqcxt.onion/10.1152/ajplung.00333.2007 C5926773!5926773 !18162602     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=18162602 &cmd=llinks): Failed to open stream: HTTP request failed! 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PPAR-gamma agonists inhibit profibrotic phenotypes in human lung fibroblasts and bleomycin-induced pulmonary fibrosis |pdf=|usr=}}{{18162602 }} gab.com Text PPAR-gamma 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-gamma (PPAR-gamma) 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-gamma as a potential therapeutic target for fibrotic lung diseases remains undefined. In the present study, we show expression of PPAR-gamma in fibroblasts obtained from normal human lungs and lungs of patients with idiopathic interstitial pneumonias. Treatment of lung fibroblasts and myofibroblasts with PPAR-gamma agonists results in inhibition of proliferative responses and induces cell cycle arrest. In addition, PPAR-gamma agonists, including a constitutively active PPAR-gamma construct (VP16-PPAR-gamma), inhibit the ability of transforming growth factor-beta1 to induce myofibroblast differentiation and collagen secretion. PPAR-gamma 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-gamma is an important regulator of fibroblast/myofibroblast activation and suggest a role for PPAR-gamma ligands as novel therapeutic agents for fibrotic lung diseases. Twit Text FOAVip PPAR-gamma 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-gamma 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 PMID18162602 show 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-gamma (PPAR-gamma) 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-gamma as a potential therapeutic target for fibrotic lung diseases remains undefined. In the present study, we show expression of PPAR-gamma in fibroblasts obtained from normal human lungs and lungs of patients with idiopathic interstitial pneumonias. Treatment of lung fibroblasts and myofibroblasts with PPAR-gamma agonists results in inhibition of proliferative responses and induces cell cycle arrest. In addition, PPAR-gamma agonists, including a constitutively active PPAR-gamma construct (VP16-PPAR-gamma), inhibit the ability of transforming growth factor-beta1 to induce myofibroblast differentiation and collagen secretion. PPAR-gamma 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-gamma is an important regulator of fibroblast/myofibroblast activation and suggest a role for PPAR-gamma ligands as novel therapeutic agents for fibrotic lung diseases. |Animals [MESH] |Antibiotics, Antineoplastic [MESH] |Bleomycin [MESH] |Cell Differentiation/drug effects/physiology [MESH] |Cell Division/drug effects/physiology [MESH] |Cells, Cultured [MESH] |Chromans/pharmacology [MESH] |Cyclin D [MESH] |Cyclins/genetics [MESH] |Disease Models, Animal [MESH] |Fibroblasts/*drug effects/pathology [MESH] |Fibrosis [MESH] |Gene Expression/physiology [MESH] |Humans [MESH] |Hypoglycemic Agents/*pharmacology [MESH] |Ligands [MESH] |PPAR gamma/*agonists/genetics/metabolism [MESH] |Phenotype [MESH] |Promoter Regions, Genetic/physiology [MESH] |Pulmonary Fibrosis/chemically induced/*drug therapy/pathology [MESH] |Rats [MESH] |Rats, Inbred F344 [MESH] |Thiazolidinediones/*pharmacology [MESH] |Transforming Growth Factor beta1/pharmacology [MESH]PPAR-gamma agonists inhibit profibrotic phenotypes in human lung fibro(epmc).pdf DeepDyve Pubget Overpricing