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10.1038/srep32430 http://scihub22266oqcxt.onion/10.1038/srep32430 C5006240!5006240 !27577254     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27577254 &cmd=llinks): Failed to open stream: HTTP request failed! 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Proliferation in cardiac fibroblasts induced by ?1-adrenoceptor autoantibody and the underlying mechanisms |pdf=|usr=}}{{27577254 }} gab.com Text Proliferation in cardiac fibroblasts induced by 1-adrenoceptor autoantibody and the underlying mechanisms JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27577254 #FOAvip Chronic sustained stimulation of ?-adrenoceptor is closely related to cardiac fibrosis which is bad for cardiac function. Growing evidence showed that the high prevalence of ?1-adrenoceptor autoantibody (?1-AA) in the sera of patients with various types of cardiovascular diseases decreased cardiac function. In the current study, we demonstrated that ?1-AA impaired the cardiac function evaluated by echocardiography and that ?1-AA triggered cardiac fibrosis in terms of increased expression of ?-smooth muscle actin as the marker of myofibroblast and collagen deposition in a passive ?1-AA immunized mice model during 16 weeks. Further, we showed that ?1-AA activated ?1-AR/cAMP/PKA pathway and promoted proliferation in primary cardiac fibroblasts through specific binding to ?1-AR but not to ?2-AR. Moreover, ?1-AA was also likely to promote proliferation in cardiac fibroblasts through activating p38MAPK and ERK1/2 as p38MAPK inhibitor SB203580 and ERK1/2 inhibitor PD98059 partially reversed the proliferative effect. The persistent activating signalling of PKA and P38MAPK in 1?h induced by ?1-AA was associated with lacking agonist-induced desensitization phenomena. The conditioned medium from ?1-AA-stimulated cardiac fibroblasts induced cardiomyocyte apoptosis, which indicated that ?1-AA changed the secretion of cardiac fibroblasts contributing to cardiac injury. These findings will contribute to our understanding of the pathological mechanisms of ?1-AA. Twit Text FOAVip Proliferation in cardiac fibroblasts induced by 1-adrenoceptor autoantibody and the underlying mechanisms ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27577254 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27577254 #FOAvip English Wikipedia <ref>{{Cite pmid|27577254 }}</ref> Proliferation in cardiac fibroblasts induced by ?1-adrenoceptor autoantibody and the underlying mechanisms #MMPMID27577254 Lv T ; Du Y ; Cao N ; Zhang S ; Gong Y ; Bai Y ; Wang W ; Liu H Sci Rep 2016[Aug]; 6 (ä): 32430 PMID27577254 show ga Chronic sustained stimulation of ?-adrenoceptor is closely related to cardiac fibrosis which is bad for cardiac function. Growing evidence showed that the high prevalence of ?1-adrenoceptor autoantibody (?1-AA) in the sera of patients with various types of cardiovascular diseases decreased cardiac function. In the current study, we demonstrated that ?1-AA impaired the cardiac function evaluated by echocardiography and that ?1-AA triggered cardiac fibrosis in terms of increased expression of ?-smooth muscle actin as the marker of myofibroblast and collagen deposition in a passive ?1-AA immunized mice model during 16 weeks. Further, we showed that ?1-AA activated ?1-AR/cAMP/PKA pathway and promoted proliferation in primary cardiac fibroblasts through specific binding to ?1-AR but not to ?2-AR. Moreover, ?1-AA was also likely to promote proliferation in cardiac fibroblasts through activating p38MAPK and ERK1/2 as p38MAPK inhibitor SB203580 and ERK1/2 inhibitor PD98059 partially reversed the proliferative effect. The persistent activating signalling of PKA and P38MAPK in 1?h induced by ?1-AA was associated with lacking agonist-induced desensitization phenomena. The conditioned medium from ?1-AA-stimulated cardiac fibroblasts induced cardiomyocyte apoptosis, which indicated that ?1-AA changed the secretion of cardiac fibroblasts contributing to cardiac injury. These findings will contribute to our understanding of the pathological mechanisms of ?1-AA. |Actins/genetics/immunology [MESH] |Amino Acid Sequence [MESH] |Animals [MESH] |Animals, Newborn [MESH] |Autoantibodies/administration & dosage/biosynthesis [MESH] |Cell Line [MESH] |Cell Proliferation/drug effects [MESH] |Echocardiography [MESH] |Endomyocardial Fibrosis/etiology/genetics/*immunology/pathology [MESH] |Fibroblasts/drug effects/*immunology/pathology [MESH] |Flavonoids/pharmacology [MESH] |Gene Expression Regulation [MESH] |Imidazoles/pharmacology [MESH] |Immunization, Passive [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mitogen-Activated Protein Kinase 1/antagonists & inhibitors/genetics/immunology [MESH] |Mitogen-Activated Protein Kinase 3/antagonists & inhibitors/genetics/immunology [MESH] |Myocardium/*immunology/pathology [MESH] |Myocytes, Cardiac/drug effects/*immunology/pathology [MESH] |Primary Cell Culture [MESH] |Pyridines/pharmacology [MESH] |Rats [MESH] |Receptors, Adrenergic, beta-1/*genetics/immunology [MESH] |Signal Transduction [MESH]Proliferation in cardiac fibroblasts induced by ?1-adrenoceptor autoan(epmc).pdf DeepDyve Pubget Overpricing