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10.1016/j.joca.2014.11.012 http://scihub22266oqcxt.onion/10.1016/j.joca.2014.11.012 C4465392!4465392!25464168     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Osteoarthritis+Cartilage 2015 ; 23 (2): 308-18 Nephropedia Template TP {{tp|p=25464168|t=2015. Lysophosphatidic Acid Mediates Fibrosis In Injured Joints By Regulating Collagen Type I Biosynthesis |pdf=|usr=}}{{25464168}} gab.com Text Lysophosphatidic Acid Mediates Fibrosis In Injured Joints By Regulating Collagen Type I Biosynthesis JO: Osteoarthritis Cartilage http://www.kidney.de/pget.php?&tw=1&pmid=25464168 #FOAvip Objective: Articular cartilage is a highly specialized tissue which forms the surfaces in synovial joints. Full-thickness cartilage defects caused by trauma or microfracture surgery heal via the formation of fibrotic tissue characterized by a high content of collagen I (COL I) and subsequent poor mechanical properties. The goal of this study is to investigate the molecular mechanisms underlying fibrosis after joint injury. Design: Rat knee joint models are used to mimic cartilage defects after acute injury. Immunohistochemistry was performed to detect proteins related to fibrosis. Human fetal chondroyges and bone marrow stromal cells (BMSCs) were used to study the influence of lipid lysophosphatidic acid (LPA) on Collagen I (COL I) synthesis. Quantitative PCR, ELISA and immunohistochemistry were performed to evaluate the productions of COL I. Chemical inhibitors were used to block LPA signaling both in vitro and in vivo. Results: After full-thickness cartilage injury in rat knee joints, stromal cells migrating to the injury expressed high levels of the LPA-producing enzyme autotaxin (ATX); intact articular cartilage in rat and humans expressed negligible levels of ATX despite expressing the LPA receptors LPAR1 and LPAR2. LPA-induced increases in COL I production by chondrocytes and BMSCs was mediated via the MAP kinase (MAPK) and PI3 Kinase (PI3K) signaling pathways. Inhibition of the ATX/LPA axis significantly reduced COL I-enriched fibrocartilage synthesis in full-thickness cartilage defects in rats in favor of the collagen II-enriched normal state. Conclusion: Taken together, these results identify an attractive target for intervention in reducing the progression of post-traumatic osteoarthritis. Twit Text FOAVip Lysophosphatidic Acid Mediates Fibrosis In Injured Joints By Regulating Collagen Type I Biosynthesis ????Osteoarthritis Cartilage http://www.kidney.de/pget.php?&tw=1&pmid=25464168 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25464168 #FOAvip English Wikipedia <ref>{{Cite pmid|25464168}}</ref> Lysophosphatidic Acid Mediates Fibrosis In Injured Joints By Regulating Collagen Type I Biosynthesis #MMPMID25464168 Wu L; Petrigliano FA; Ba K; Lee S; Bogdanov J; McAllister DR; Adams JS; Rosenthal AK; Van Handel B; Crooks GM; Lin Y; Evseenko D Osteoarthritis Cartilage 2015[Feb]; 23 (2): 308-18 PMID25464168show ga Objective: Articular cartilage is a highly specialized tissue which forms the surfaces in synovial joints. Full-thickness cartilage defects caused by trauma or microfracture surgery heal via the formation of fibrotic tissue characterized by a high content of collagen I (COL I) and subsequent poor mechanical properties. The goal of this study is to investigate the molecular mechanisms underlying fibrosis after joint injury. Design: Rat knee joint models are used to mimic cartilage defects after acute injury. Immunohistochemistry was performed to detect proteins related to fibrosis. Human fetal chondroyges and bone marrow stromal cells (BMSCs) were used to study the influence of lipid lysophosphatidic acid (LPA) on Collagen I (COL I) synthesis. Quantitative PCR, ELISA and immunohistochemistry were performed to evaluate the productions of COL I. Chemical inhibitors were used to block LPA signaling both in vitro and in vivo. Results: After full-thickness cartilage injury in rat knee joints, stromal cells migrating to the injury expressed high levels of the LPA-producing enzyme autotaxin (ATX); intact articular cartilage in rat and humans expressed negligible levels of ATX despite expressing the LPA receptors LPAR1 and LPAR2. LPA-induced increases in COL I production by chondrocytes and BMSCs was mediated via the MAP kinase (MAPK) and PI3 Kinase (PI3K) signaling pathways. Inhibition of the ATX/LPA axis significantly reduced COL I-enriched fibrocartilage synthesis in full-thickness cartilage defects in rats in favor of the collagen II-enriched normal state. Conclusion: Taken together, these results identify an attractive target for intervention in reducing the progression of post-traumatic osteoarthritis. äLysophosphatidic Acid Mediates Fibrosis In Injured Joints By Regulatin(epmc).pdf DeepDyve Pubget Overpricing