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10.1073/pnas.1415111112 http://scihub22266oqcxt.onion/10.1073/pnas.1415111112 C4413321!4413321 !25848047     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25848047 &cmd=llinks): Failed to open stream: HTTP request failed! 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Compromised peroxisomes in idiopathic pulmonary fibrosis, a vicious cycle inducing a higher fibrotic response via TGF-? signaling |pdf=|usr=}}{{25848047 }} gab.com Text Compromised peroxisomes in idiopathic pulmonary fibrosis, a vicious cycle inducing a higher fibrotic response via TGF- signaling JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25848047 #FOAvip Idiopathic pulmonary fibrosis (IPF) is a devastating disease, and its pathogenic mechanisms remain incompletely understood. Peroxisomes are known to be important in ROS and proinflammatory lipid degradation, and their deficiency induces liver fibrosis. However, altered peroxisome functions in IPF pathogenesis have never been investigated. By comparing peroxisome-related protein and gene expression in lung tissue and isolated lung fibroblasts between human control and IPF patients, we found that IPF lungs exhibited a significant down-regulation of peroxisomal biogenesis and metabolism (e.g., PEX13p and acyl-CoA oxidase 1). Moreover, in vivo the bleomycin-induced down-regulation of peroxisomes was abrogated in transforming growth factor beta (TGF-?) receptor II knockout mice indicating a role for TGF-? signaling in the regulation of peroxisomes. Furthermore, in vitro treatment of IPF fibroblasts with the profibrotic factors TGF-?1 or tumor necrosis factor alpha (TNF-?) was found to down-regulate peroxisomes via the AP-1 signaling pathway. Therefore, the molecular mechanisms by which reduced peroxisomal functions contribute to enhanced fibrosis were further studied. Direct down-regulation of PEX13 by RNAi induced the activation of Smad-dependent TGF-? signaling accompanied by increased ROS production and resulted in the release of cytokines (e.g., IL-6, TGF-?) and excessive production of collagen I and III. In contrast, treatment of fibroblasts with ciprofibrate or WY14643, PPAR-? activators, led to peroxisome proliferation and reduced the TGF-?-induced myofibroblast differentiation and collagen protein in IPF cells. Taken together, our findings suggest that compromised peroxisome activity might play an important role in the molecular pathogenesis of IPF and fibrosis progression, possibly by exacerbating pulmonary inflammation and intensifying the fibrotic response in the patients. Twit Text FOAVip Compromised peroxisomes in idiopathic pulmonary fibrosis, a vicious cycle inducing a higher fibrotic response via TGF- signaling ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25848047 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25848047 #FOAvip English Wikipedia <ref>{{Cite pmid|25848047 }}</ref> Compromised peroxisomes in idiopathic pulmonary fibrosis, a vicious cycle inducing a higher fibrotic response via TGF-? signaling #MMPMID25848047 Oruqaj G ; Karnati S ; Vijayan V ; Kotarkonda LK ; Boateng E ; Zhang W ; Ruppert C ; Günther A ; Shi W ; Baumgart-Vogt E Proc Natl Acad Sci U S A 2015[Apr]; 112 (16 ): E2048-57 PMID25848047 show ga Idiopathic pulmonary fibrosis (IPF) is a devastating disease, and its pathogenic mechanisms remain incompletely understood. Peroxisomes are known to be important in ROS and proinflammatory lipid degradation, and their deficiency induces liver fibrosis. However, altered peroxisome functions in IPF pathogenesis have never been investigated. By comparing peroxisome-related protein and gene expression in lung tissue and isolated lung fibroblasts between human control and IPF patients, we found that IPF lungs exhibited a significant down-regulation of peroxisomal biogenesis and metabolism (e.g., PEX13p and acyl-CoA oxidase 1). Moreover, in vivo the bleomycin-induced down-regulation of peroxisomes was abrogated in transforming growth factor beta (TGF-?) receptor II knockout mice indicating a role for TGF-? signaling in the regulation of peroxisomes. Furthermore, in vitro treatment of IPF fibroblasts with the profibrotic factors TGF-?1 or tumor necrosis factor alpha (TNF-?) was found to down-regulate peroxisomes via the AP-1 signaling pathway. Therefore, the molecular mechanisms by which reduced peroxisomal functions contribute to enhanced fibrosis were further studied. Direct down-regulation of PEX13 by RNAi induced the activation of Smad-dependent TGF-? signaling accompanied by increased ROS production and resulted in the release of cytokines (e.g., IL-6, TGF-?) and excessive production of collagen I and III. In contrast, treatment of fibroblasts with ciprofibrate or WY14643, PPAR-? activators, led to peroxisome proliferation and reduced the TGF-?-induced myofibroblast differentiation and collagen protein in IPF cells. Taken together, our findings suggest that compromised peroxisome activity might play an important role in the molecular pathogenesis of IPF and fibrosis progression, possibly by exacerbating pulmonary inflammation and intensifying the fibrotic response in the patients. |*Signal Transduction [MESH] |Animals [MESH] |Collagen Type I/metabolism [MESH] |Disease Models, Animal [MESH] |Down-Regulation [MESH] |Female [MESH] |Fibroblasts/metabolism/pathology [MESH] |Gene Knockdown Techniques [MESH] |Humans [MESH] |Idiopathic Pulmonary Fibrosis/*metabolism/*pathology [MESH] |Inflammation Mediators/metabolism [MESH] |Interleukin-6/metabolism [MESH] |Lipid Metabolism [MESH] |Lung/pathology [MESH] |Male [MESH] |Membrane Proteins/metabolism [MESH] |Mice, Inbred C57BL [MESH] |Middle Aged [MESH] |Models, Biological [MESH] |Oxidation-Reduction [MESH] |PPAR alpha/agonists/metabolism [MESH] |Peroxisomes/*metabolism [MESH] |RNA, Small Interfering/metabolism [MESH] |Reactive Oxygen Species/metabolism [MESH] |Smad Proteins/metabolism [MESH] |Transcription Factor AP-1/metabolism [MESH] |Transforming Growth Factor beta/*metabolism [MESH]Compromised peroxisomes in idiopathic pulmonary fibrosis, a vicious cy(epmc).pdf DeepDyve Pubget Overpricing