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10.1038/s41598-017-00418-y http://scihub22266oqcxt.onion/10.1038/s41598-017-00418-y C5428408!5428408 !28336948     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28336948 &cmd=llinks): Failed to open stream: HTTP request failed! 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Plasminogen Activator Inhibitor-1 Protects Mice Against Cardiac Fibrosis by Inhibiting Urokinase-type Plasminogen Activator-mediated Plasminogen Activation |pdf=|usr=}}{{28336948 }} gab.com Text Plasminogen Activator Inhibitor-1 Protects Mice Against Cardiac Fibrosis by Inhibiting Urokinase-type Plasminogen Activator-mediated Plasminogen Activation JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28336948 #FOAvip Plasminogen activator inhibitor-1 (PAI-1) is known to protect mice against cardiac fibrosis. It has been speculated that PAI-1 may regulate cardiac fibrosis by inactivating urokinase-type plasminogen activator (uPA) and ultimately plasmin (Pm) generation. However, the in vivo role of PAI-1 in inactivating uPA and limiting the generation of Pm during cardiac fibrosis remains to be established. The objective of this study was to determine if the cardioprotective effect of PAI-1 is mediated through its ability to directly regulate urokinase -mediated activation of plasminogen (Pg). An Angiotensin II (AngII)-aldosterone (Ald) infusion mouse model of hypertension was utilised in this study. Four weeks after AngII-Ald infusion, PAI-1-deficient (PAI-1(-/-)) mice developed severe cardiac fibrosis. However, a marked reduction in cardiac fibrosis was observed in PAI-1(-/-)/uPA(-/-) double knockout mice that was associated with reduced inflammation, lower expression levels of TGF-? and proteases associated with tissue remodeling, and diminished Smad2 signaling. Moreover, total ablation of cardiac fibrosis was observed in PAI-1(-/-) mice that express inactive plasmin (Pm) but normal levels of zymogen Pg (PAI-1(-/-)/Pg(S743A/S743A)). Our findings indicate that PAI-1 protects mice from hypertension-induced cardiac fibrosis by inhibiting the generation of active Pm. Twit Text FOAVip Plasminogen Activator Inhibitor-1 Protects Mice Against Cardiac Fibrosis by Inhibiting Urokinase-type Plasminogen Activator-mediated Plasminogen Activation ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28336948 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28336948 #FOAvip English Wikipedia <ref>{{Cite pmid|28336948 }}</ref> Plasminogen Activator Inhibitor-1 Protects Mice Against Cardiac Fibrosis by Inhibiting Urokinase-type Plasminogen Activator-mediated Plasminogen Activation #MMPMID28336948 Gupta KK ; Donahue DL ; Sandoval-Cooper MJ ; Castellino FJ ; Ploplis VA Sci Rep 2017[Mar]; 7 (1 ): 365 PMID28336948 show ga Plasminogen activator inhibitor-1 (PAI-1) is known to protect mice against cardiac fibrosis. It has been speculated that PAI-1 may regulate cardiac fibrosis by inactivating urokinase-type plasminogen activator (uPA) and ultimately plasmin (Pm) generation. However, the in vivo role of PAI-1 in inactivating uPA and limiting the generation of Pm during cardiac fibrosis remains to be established. The objective of this study was to determine if the cardioprotective effect of PAI-1 is mediated through its ability to directly regulate urokinase -mediated activation of plasminogen (Pg). An Angiotensin II (AngII)-aldosterone (Ald) infusion mouse model of hypertension was utilised in this study. Four weeks after AngII-Ald infusion, PAI-1-deficient (PAI-1(-/-)) mice developed severe cardiac fibrosis. However, a marked reduction in cardiac fibrosis was observed in PAI-1(-/-)/uPA(-/-) double knockout mice that was associated with reduced inflammation, lower expression levels of TGF-? and proteases associated with tissue remodeling, and diminished Smad2 signaling. Moreover, total ablation of cardiac fibrosis was observed in PAI-1(-/-) mice that express inactive plasmin (Pm) but normal levels of zymogen Pg (PAI-1(-/-)/Pg(S743A/S743A)). Our findings indicate that PAI-1 protects mice from hypertension-induced cardiac fibrosis by inhibiting the generation of active Pm. |Animals [MESH] |Disease Models, Animal [MESH] |Fibrinolysin/*metabolism [MESH] |Fibrosis [MESH] |Gene Expression [MESH] |Heart Diseases/*enzymology/etiology/*pathology [MESH] |Hypertension/complications [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Myocardium/metabolism/pathology [MESH] |Phenotype [MESH] |Plasminogen Activator Inhibitor 1/genetics/*metabolism [MESH] |Plasminogen/*metabolism [MESH] |Smad2 Protein/metabolism [MESH]Plasminogen Activator Inhibitor-1 Protects Mice Against Cardiac Fibros(epmc).pdf DeepDyve Pubget Overpricing