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10.1165/rcmb.2013-0092OC http://scihub22266oqcxt.onion/10.1165/rcmb.2013-0092OC C4068920!4068920 !24175906     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24175906 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibition of transglutaminase 2, a novel target for pulmonary fibrosis, by two small electrophilic molecules |pdf=|usr=}}{{24175906 }} gab.com Text Inhibition of transglutaminase 2, a novel target for pulmonary fibrosis, by two small electrophilic molecules JO: Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=24175906 #FOAvip Idiopathic pulmonary fibrosis (IPF) is characterized by progressive fibrotic destruction of normal lung architecture. Due to a lack of effective treatment options, new treatment approaches are needed. We previously identified transglutaminase (TG)2, a multifunctional protein expressed by human lung fibroblasts (HLFs), as a positive driver of fibrosis. TG2 catalyzes crosslinking of extracellular matrix proteins, enhances cell binding to fibronectin and integrin, and promotes fibronectin expression. We investigated whether the small electrophilic molecules 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) and 15-deoxy-delta-12,14-prostaglandin J2 (15d-PGJ2) inhibit the expression and profibrotic functions of TG2. CDDO and 15d-PGJ2 reduced expression of TG2 mRNA and protein in primary HLFs from control donors and donors with IPF. CDDO and 15d-PGJ2 also decreased the in vitro profibrotic effector functions of HLFs including collagen gel contraction and cell migration. The decrease in TG2 expression did not occur through activation of the peroxisome proliferator activated receptor ? or generation of reactive oxidative species. CDDO and 15d-PGJ2 inhibited the extracellular signal-regulated kinase pathway, resulting in the suppression of TG2 expression. This is the first study to show that small electrophilic compounds inhibit the expression and profibrotic effector functions of TG2, a key promoter of fibrosis. These studies identify new and important antifibrotic activities of these two small molecules, which could lead to new treatments for fibrotic lung disease. Twit Text FOAVip Inhibition of transglutaminase 2, a novel target for pulmonary fibrosis, by two small electrophilic molecules ????Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=24175906 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24175906 #FOAvip English Wikipedia <ref>{{Cite pmid|24175906 }}</ref> Inhibition of transglutaminase 2, a novel target for pulmonary fibrosis, by two small electrophilic molecules #MMPMID24175906 Olsen KC ; Epa AP ; Kulkarni AA ; Kottmann RM ; McCarthy CE ; Johnson GV ; Thatcher TH ; Phipps RP ; Sime PJ Am J Respir Cell Mol Biol 2014[Apr]; 50 (4 ): 737-47 PMID24175906 show ga Idiopathic pulmonary fibrosis (IPF) is characterized by progressive fibrotic destruction of normal lung architecture. Due to a lack of effective treatment options, new treatment approaches are needed. We previously identified transglutaminase (TG)2, a multifunctional protein expressed by human lung fibroblasts (HLFs), as a positive driver of fibrosis. TG2 catalyzes crosslinking of extracellular matrix proteins, enhances cell binding to fibronectin and integrin, and promotes fibronectin expression. We investigated whether the small electrophilic molecules 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) and 15-deoxy-delta-12,14-prostaglandin J2 (15d-PGJ2) inhibit the expression and profibrotic functions of TG2. CDDO and 15d-PGJ2 reduced expression of TG2 mRNA and protein in primary HLFs from control donors and donors with IPF. CDDO and 15d-PGJ2 also decreased the in vitro profibrotic effector functions of HLFs including collagen gel contraction and cell migration. The decrease in TG2 expression did not occur through activation of the peroxisome proliferator activated receptor ? or generation of reactive oxidative species. CDDO and 15d-PGJ2 inhibited the extracellular signal-regulated kinase pathway, resulting in the suppression of TG2 expression. This is the first study to show that small electrophilic compounds inhibit the expression and profibrotic effector functions of TG2, a key promoter of fibrosis. These studies identify new and important antifibrotic activities of these two small molecules, which could lead to new treatments for fibrotic lung disease. |Case-Control Studies [MESH] |Cell Movement/drug effects [MESH] |Cell Shape/drug effects [MESH] |Cells, Cultured [MESH] |Dose-Response Relationship, Drug [MESH] |Down-Regulation [MESH] |Enzyme Inhibitors/chemistry/*pharmacology [MESH] |Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/metabolism [MESH] |Fibroblasts/drug effects/enzymology/pathology [MESH] |GTP-Binding Proteins [MESH] |Humans [MESH] |Idiopathic Pulmonary Fibrosis/*enzymology/pathology [MESH] |Lung/*drug effects/enzymology/pathology [MESH] |MAP Kinase Kinase Kinases/antagonists & inhibitors/metabolism [MESH] |MAP Kinase Signaling System/drug effects [MESH] |Molecular Targeted Therapy [MESH] |Oleanolic Acid/*analogs & derivatives/chemistry/pharmacology [MESH] |Phosphorylation [MESH] |Prostaglandin D2/*analogs & derivatives/chemistry/pharmacology [MESH] |Protein Glutamine gamma Glutamyltransferase 2 [MESH] |Protein Kinase Inhibitors/pharmacology [MESH]Inhibition of transglutaminase 2, a novel target for pulmonary fibrosi(epmc).pdf DeepDyve Pubget Overpricing