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10.1164/rccm.201310-1917OC http://scihub22266oqcxt.onion/10.1164/rccm.201310-1917OC C4098083!4098083 !24779708     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24779708 &cmd=llinks): Failed to open stream: HTTP request failed! 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The mitochondrial cardiolipin remodeling enzyme lysocardiolipin acyltransferase is a novel target in pulmonary fibrosis |pdf=|usr=}}{{24779708 }} gab.com Text The mitochondrial cardiolipin remodeling enzyme lysocardiolipin acyltransferase is a novel target in pulmonary fibrosis JO: Am J Respir Crit Care Med http://www.kidney.de/pget.php?&tw=1&pmid=24779708 #FOAvip RATIONALE: Lysocardiolipin acyltransferase (LYCAT), a cardiolipin-remodeling enzyme regulating the 18:2 linoleic acid pattern of mammalian mitochondrial cardiolipin, is necessary for maintaining normal mitochondrial function and vascular development. We hypothesized that modulation of LYCAT expression in lung epithelium regulates development of pulmonary fibrosis. OBJECTIVES: To define a role for LYCAT in human and murine models of pulmonary fibrosis. METHODS: We analyzed the correlation of LYCAT expression in peripheral blood mononuclear cells (PBMCs) with the outcomes of pulmonary functions and overall survival, and used the murine models to establish the role of LYCAT in fibrogenesis. We studied the LYCAT action on cardiolipin remodeling, mitochondrial reactive oxygen species generation, and apoptosis of alveolar epithelial cells under bleomycin challenge. MEASUREMENTS AND MAIN RESULTS: LYCAT expression was significantly altered in PBMCs and lung tissues from patients with idiopathic pulmonary fibrosis (IPF), which was confirmed in two preclinical murine models of IPF, bleomycin- and radiation-induced pulmonary fibrosis. LYCAT mRNA expression in PBMCs directly and significantly correlated with carbon monoxide diffusion capacity, pulmonary function outcomes, and overall survival. In both bleomycin- and radiation-induced pulmonary fibrosis murine models, hLYCAT overexpression reduced several indices of lung fibrosis, whereas down-regulation of native LYCAT expression by siRNA accentuated fibrogenesis. In vitro studies demonstrated that LYCAT modulated bleomycin-induced cardiolipin remodeling, mitochondrial membrane potential, reactive oxygen species generation, and apoptosis of alveolar epithelial cells, potential mechanisms of LYCAT-mediated lung protection. CONCLUSIONS: This study is the first to identify modulation of LYCAT expression in fibrotic lungs and offers a novel therapeutic approach for ameliorating lung inflammation and pulmonary fibrosis. Twit Text FOAVip The mitochondrial cardiolipin remodeling enzyme lysocardiolipin acyltransferase is a novel target in pulmonary fibrosis ????Am J Respir Crit Care Med http://www.kidney.de/pget.php?&tw=1&pmid=24779708 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24779708 #FOAvip English Wikipedia <ref>{{Cite pmid|24779708 }}</ref> The mitochondrial cardiolipin remodeling enzyme lysocardiolipin acyltransferase is a novel target in pulmonary fibrosis #MMPMID24779708 Huang LS ; Mathew B ; Li H ; Zhao Y ; Ma SF ; Noth I ; Reddy SP ; Harijith A ; Usatyuk PV ; Berdyshev EV ; Kaminski N ; Zhou T ; Zhang W ; Zhang Y ; Rehman J ; Kotha SR ; Gurney TO ; Parinandi NL ; Lussier YA ; Garcia JG ; Natarajan V Am J Respir Crit Care Med 2014[Jun]; 189 (11 ): 1402-15 PMID24779708 show ga RATIONALE: Lysocardiolipin acyltransferase (LYCAT), a cardiolipin-remodeling enzyme regulating the 18:2 linoleic acid pattern of mammalian mitochondrial cardiolipin, is necessary for maintaining normal mitochondrial function and vascular development. We hypothesized that modulation of LYCAT expression in lung epithelium regulates development of pulmonary fibrosis. OBJECTIVES: To define a role for LYCAT in human and murine models of pulmonary fibrosis. METHODS: We analyzed the correlation of LYCAT expression in peripheral blood mononuclear cells (PBMCs) with the outcomes of pulmonary functions and overall survival, and used the murine models to establish the role of LYCAT in fibrogenesis. We studied the LYCAT action on cardiolipin remodeling, mitochondrial reactive oxygen species generation, and apoptosis of alveolar epithelial cells under bleomycin challenge. MEASUREMENTS AND MAIN RESULTS: LYCAT expression was significantly altered in PBMCs and lung tissues from patients with idiopathic pulmonary fibrosis (IPF), which was confirmed in two preclinical murine models of IPF, bleomycin- and radiation-induced pulmonary fibrosis. LYCAT mRNA expression in PBMCs directly and significantly correlated with carbon monoxide diffusion capacity, pulmonary function outcomes, and overall survival. In both bleomycin- and radiation-induced pulmonary fibrosis murine models, hLYCAT overexpression reduced several indices of lung fibrosis, whereas down-regulation of native LYCAT expression by siRNA accentuated fibrogenesis. In vitro studies demonstrated that LYCAT modulated bleomycin-induced cardiolipin remodeling, mitochondrial membrane potential, reactive oxygen species generation, and apoptosis of alveolar epithelial cells, potential mechanisms of LYCAT-mediated lung protection. CONCLUSIONS: This study is the first to identify modulation of LYCAT expression in fibrotic lungs and offers a novel therapeutic approach for ameliorating lung inflammation and pulmonary fibrosis. |1-Acylglycerol-3-Phosphate O-Acyltransferase/*genetics [MESH] |Acyltransferases/*genetics [MESH] |Animals [MESH] |Biomarkers/metabolism [MESH] |Cardiolipins/genetics [MESH] |Cohort Studies [MESH] |Disease Models, Animal [MESH] |Humans [MESH] |Idiopathic Pulmonary Fibrosis/diagnosis/genetics [MESH] |In Situ Hybridization [MESH] |Leukocytes, Mononuclear/metabolism [MESH] |Mice [MESH] |Mitochondria/*genetics/metabolism [MESH] |Predictive Value of Tests [MESH] |Pulmonary Fibrosis/*diagnosis/enzymology/*genetics [MESH] |RNA, Messenger/metabolism [MESH] |Sensitivity and Specificity [MESH]The mitochondrial cardiolipin remodeling enzyme lysocardiolipin acyltr(epmc).pdf DeepDyve Pubget Overpricing