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10.1161/JAHA.118.010418 http://scihub22266oqcxt.onion/10.1161/JAHA.118.010418 30563389!6405723!30563389     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30563389&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       J+Am+Heart+Assoc 2019 ; 8 (1): e010418 Nephropedia Template TP {{tp|p=30563389|t=2019. K(Ca)3 1 Channels Promote Cardiac Fibrosis Through Mediating Inflammation and Differentiation of Monocytes Into Myofibroblasts in Angiotensin II -Treated Rats |pdf=|usr=}}{{30563389}} gab.com Text K(Ca)3 1 Channels Promote Cardiac Fibrosis Through Mediating Inflammation and Differentiation of Monocytes Into Myofibroblasts in Angiotensin II -Treated Rats JO: J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=30563389 #FOAvip Background Cardiac fibrosis is a core pathological process associated with heart failure. The recruitment and differentiation of primitive fibroblast precursor cells of bone marrow origin play a critical role in pathological interstitial cardiac fibrosis. The K(C)(a)3.1 channels are expressed in both ventricular fibroblasts and circulating mononuclear cells in rats and are upregulated by angiotensin II . We hypothesized that K(C)(a)3.1 channels mediate the inflammatory microenvironment in the heart, promoting the infiltrated bone marrow-derived circulating mononuclear cells to differentiate into myofibroblasts, leading to myocardial fibrosis. Methods and Results We established a cardiac fibrosis model in rats by infusing angiotensin II to evaluate the impact of the specific K(C)(a)3.1 channel blocker TRAM -34 on cardiac fibrosis. At the same time, mouse CD 4(+) T cells and rat circulating mononuclear cells were separated to investigate the underlying mechanism of the TRAM -34 anti-cardiac fibrosis effect. TRAM -34 significantly attenuated cardiac fibrosis and the inflammatory reaction and reduced the number of fibroblast precursor cells and myofibroblasts. Inhibition of K(C)(a)3.1 channels suppressed angiotensin II -stimulated expression and secretion of interleukin-4 and interleukin-13 in CD 4(+) T cells and interleukin-4- or interleukin-13-induced differentiation of monocytes into fibrocytes. Conclusions K(C)(a)3.1 channels facilitate myocardial inflammation and the differentiation of bone marrow-derived monocytes into myofibroblasts in cardiac fibrosis caused by angiotensin II infusion. Twit Text FOAVip K(Ca)3 1 Channels Promote Cardiac Fibrosis Through Mediating Inflammation and Differentiation of Monocytes Into Myofibroblasts in Angiotensin II -Treated Rats ????J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=30563389 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30563389 #FOAvip English Wikipedia <ref>{{Cite pmid|30563389}}</ref> K(Ca)3 1 Channels Promote Cardiac Fibrosis Through Mediating Inflammation and Differentiation of Monocytes Into Myofibroblasts in Angiotensin II -Treated Rats #MMPMID30563389 She G; Ren YJ; Wang Y; Hou MC; Wang HF; Gou W; Lai BC; Lei T; Du XJ; Deng XL J Am Heart Assoc 2019[Jan]; 8 (1): e010418 PMID30563389show ga Background Cardiac fibrosis is a core pathological process associated with heart failure. The recruitment and differentiation of primitive fibroblast precursor cells of bone marrow origin play a critical role in pathological interstitial cardiac fibrosis. The K(C)(a)3.1 channels are expressed in both ventricular fibroblasts and circulating mononuclear cells in rats and are upregulated by angiotensin II . We hypothesized that K(C)(a)3.1 channels mediate the inflammatory microenvironment in the heart, promoting the infiltrated bone marrow-derived circulating mononuclear cells to differentiate into myofibroblasts, leading to myocardial fibrosis. Methods and Results We established a cardiac fibrosis model in rats by infusing angiotensin II to evaluate the impact of the specific K(C)(a)3.1 channel blocker TRAM -34 on cardiac fibrosis. At the same time, mouse CD 4(+) T cells and rat circulating mononuclear cells were separated to investigate the underlying mechanism of the TRAM -34 anti-cardiac fibrosis effect. TRAM -34 significantly attenuated cardiac fibrosis and the inflammatory reaction and reduced the number of fibroblast precursor cells and myofibroblasts. Inhibition of K(C)(a)3.1 channels suppressed angiotensin II -stimulated expression and secretion of interleukin-4 and interleukin-13 in CD 4(+) T cells and interleukin-4- or interleukin-13-induced differentiation of monocytes into fibrocytes. Conclusions K(C)(a)3.1 channels facilitate myocardial inflammation and the differentiation of bone marrow-derived monocytes into myofibroblasts in cardiac fibrosis caused by angiotensin II infusion. |*Gene Expression Regulation[MESH] |Angiotensin II/toxicity[MESH] |Animals[MESH] |Blotting, Western[MESH] |Cardiomyopathies/*genetics/metabolism/pathology[MESH] |Fibroblasts/metabolism/pathology[MESH] |Fibrosis/genetics/metabolism/pathology[MESH] |Heart Ventricles/metabolism/pathology[MESH] |Immunohistochemistry[MESH] |Inflammation/*genetics/metabolism/pathology[MESH] |Intermediate-Conductance Calcium-Activated Potassium Channels/biosynthesis/*genetics[MESH] |Male[MESH] |Monocytes/metabolism/*pathology[MESH] |Myocardium/*metabolism/pathology[MESH] |Myofibroblasts/metabolism/pathology[MESH] |RNA/genetics[MESH] |Rats[MESH]K(Ca)3 1 Channels Promote Cardiac Fibrosis Through Mediating Inflammat(epmc).pdf DeepDyve Pubget Overpricing