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10.1074/jbc.M116.724138 http://scihub22266oqcxt.onion/10.1074/jbc.M116.724138 C5016681!5016681 !27466370     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27466370 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cardiac-restricted Overexpression of TRAF3 Interacting Protein 2 (TRAF3IP2) Results in Spontaneous Development of Myocardial Hypertrophy, Fibrosis, and Dysfunction |pdf=|usr=}}{{27466370 }} gab.com Text Cardiac-restricted Overexpression of TRAF3 Interacting Protein 2 (TRAF3IP2) Results in Spontaneous Development of Myocardial Hypertrophy, Fibrosis, and Dysfunction JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27466370 #FOAvip TRAF3IP2 (TRAF3 interacting protein 2; previously known as CIKS or Act1) is a key intermediate in the normal inflammatory response and the pathogenesis of various autoimmune and inflammatory diseases. Induction of TRAF3IP2 activates I?B kinase (IKK)/NF-?B, JNK/AP-1, and c/EBP? and stimulates the expression of various inflammatory mediators with negative myocardial inotropic effects. To investigate the role of TRAF3IP2 in heart disease, we generated a transgenic mouse model with cardiomyocyte-specific TRAF3IP2 overexpression (TRAF3IP2-Tg). Echocardiography, magnetic resonance imaging, and pressure-volume conductance catheterization revealed impaired cardiac function in 2-month-old male transgenic (Tg) mice as evidenced by decreased ejection fraction, stroke volume, cardiac output, and peak ejection rate. Moreover, the male Tg mice spontaneously developed myocardial hypertrophy (increased heart/body weight ratio, cardiomyocyte cross-sectional area, GATA4 induction, and fetal gene re-expression). Furthermore, TRAF3IP2 overexpression resulted in the activation of IKK/NF-?B, JNK/AP-1, c/EBP?, and p38 MAPK and induction of proinflammatory cytokines, chemokines, and extracellular matrix proteins in the heart. Although myocardial hypertrophy decreased with age, cardiac fibrosis (increased number of myofibroblasts and enhanced expression and deposition of fibrillar collagens) increased progressively. Despite these adverse changes, TRAF3IP2 overexpression did not result in cell death at any time period. Interestingly, despite increased mRNA expression, TRAF3IP2 protein levels and activation of its downstream signaling intermediates remained unchanged in the hearts of female Tg mice. The female Tg mice also failed to develop myocardial hypertrophy. In summary, these results demonstrate that overexpression of TRAF3IP2 in male mice is sufficient to induce myocardial hypertrophy, cardiac fibrosis, and contractile dysfunction. Twit Text FOAVip Cardiac-restricted Overexpression of TRAF3 Interacting Protein 2 (TRAF3IP2) Results in Spontaneous Development of Myocardial Hypertrophy, Fibrosis, and Dysfunction ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=27466370 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27466370 #FOAvip English Wikipedia <ref>{{Cite pmid|27466370 }}</ref> Cardiac-restricted Overexpression of TRAF3 Interacting Protein 2 (TRAF3IP2) Results in Spontaneous Development of Myocardial Hypertrophy, Fibrosis, and Dysfunction #MMPMID27466370 Yariswamy M ; Yoshida T ; Valente AJ ; Kandikattu HK ; Sakamuri SS ; Siddesha JM ; Sukhanov S ; Saifudeen Z ; Ma L ; Siebenlist U ; Gardner JD ; Chandrasekar B J Biol Chem 2016[Sep]; 291 (37 ): 19425-36 PMID27466370 show ga TRAF3IP2 (TRAF3 interacting protein 2; previously known as CIKS or Act1) is a key intermediate in the normal inflammatory response and the pathogenesis of various autoimmune and inflammatory diseases. Induction of TRAF3IP2 activates I?B kinase (IKK)/NF-?B, JNK/AP-1, and c/EBP? and stimulates the expression of various inflammatory mediators with negative myocardial inotropic effects. To investigate the role of TRAF3IP2 in heart disease, we generated a transgenic mouse model with cardiomyocyte-specific TRAF3IP2 overexpression (TRAF3IP2-Tg). Echocardiography, magnetic resonance imaging, and pressure-volume conductance catheterization revealed impaired cardiac function in 2-month-old male transgenic (Tg) mice as evidenced by decreased ejection fraction, stroke volume, cardiac output, and peak ejection rate. Moreover, the male Tg mice spontaneously developed myocardial hypertrophy (increased heart/body weight ratio, cardiomyocyte cross-sectional area, GATA4 induction, and fetal gene re-expression). Furthermore, TRAF3IP2 overexpression resulted in the activation of IKK/NF-?B, JNK/AP-1, c/EBP?, and p38 MAPK and induction of proinflammatory cytokines, chemokines, and extracellular matrix proteins in the heart. Although myocardial hypertrophy decreased with age, cardiac fibrosis (increased number of myofibroblasts and enhanced expression and deposition of fibrillar collagens) increased progressively. Despite these adverse changes, TRAF3IP2 overexpression did not result in cell death at any time period. Interestingly, despite increased mRNA expression, TRAF3IP2 protein levels and activation of its downstream signaling intermediates remained unchanged in the hearts of female Tg mice. The female Tg mice also failed to develop myocardial hypertrophy. In summary, these results demonstrate that overexpression of TRAF3IP2 in male mice is sufficient to induce myocardial hypertrophy, cardiac fibrosis, and contractile dysfunction. |*MAP Kinase Signaling System [MESH] |*Stroke Volume [MESH] |Adaptor Proteins, Signal Transducing/*biosynthesis/genetics [MESH] |Animals [MESH] |CCAAT-Enhancer-Binding Protein-beta/genetics/metabolism [MESH] |Cardiomegaly/genetics/*metabolism/pathology/*physiopathology [MESH] |Chemokines/genetics/metabolism [MESH] |Collagen/biosynthesis/genetics [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Fibrosis [MESH] |Gene Expression Regulation [MESH] |MAP Kinase Kinase 4/genetics/metabolism [MESH] |Male [MESH] |Mice [MESH] |Mice, Transgenic [MESH] |Myocardium/*metabolism/pathology [MESH] |NF-kappa B/genetics/metabolism [MESH] |Sex Characteristics [MESH] |Transcription Factor AP-1/genetics/metabolism [MESH]Cardiac-restricted Overexpression of TRAF3 Interacting Protein 2 (TRAF(epmc).pdf DeepDyve Pubget Overpricing