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10.1186/s12929-017-0367-3 http://scihub22266oqcxt.onion/10.1186/s12929-017-0367-3 C5584049!5584049 !28870220     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28870220 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Biomed+Sci 2017 ; 24 (1 ): 68 Nephropedia Template TP {{tp|p=28870220 |t=2017. The type VI adenylyl cyclase protects cardiomyocytes from ?-adrenergic stress by a PKA/STAT3-dependent pathway |pdf=|usr=}}{{28870220 }} gab.com Text The type VI adenylyl cyclase protects cardiomyocytes from -adrenergic stress by a PKA/STAT3-dependent pathway JO: J Biomed Sci http://www.kidney.de/pget.php?&tw=1&pmid=28870220 #FOAvip BACKGROUND: The type VI adenylyl cyclase (AC6) is a main contributor of cAMP production in the heart. The amino acid (aa) sequence of AC6 is highly homologous to that of another major cardiac adenylyl cyclase, AC5, except for its N-terminus (AC6-N, aa 1-86). Activation of AC6, rather than AC5, produces cardioprotective effects against heart failure, while the underlying mechanism remains to be unveiled. Using an AC6-null (AC6(-/-)) mouse and a knockin mouse with AC6-N deletion (AC6 (?N/?N)), we aimed to investigate the cardioprotective mechanism of AC6 in the heart. METHODS: Western blot analysis and immunofluorescence staining were performed to determine the intracellular distribution of AC6, AC6-?N (a truncated AC6 lacking the first 86 amino acids), and STAT3 activation. Activities of AC6 and AC6-?N in the heart were assessed by cAMP assay. Apoptosis of cardiomyocytes were evaluated by the TUNEL assay and a propidium iodine-based survival assay. Fibrosis was examined by collagen staining. RESULTS: Immunofluorescence staining revealed that cardiac AC6 was mainly anchored on the sarcolemmal membranes, while AC6-?N was redistributed to the sarcoplasmic reticulum. AC6(?N/?N) and AC6(-/-) mice had more apoptotic myocytes and cardiac remodeling than WT mice in experimental models of isoproterenol (ISO)-induced myocardial injury. Adult cardiomyocytes isolated from AC6(?N/?N) or AC6(-/-) mice survived poorly after exposure to ISO, which produced no effect on WT cardiomyocytes under the condition tested. Importantly, ISO treatment induced cardiac STAT3 phosphorylation/activation in WT mice, but not in AC6(?N/?N) and AC6(-/-) mice. Pharmacological blockage of PKA-, Src-, or STAT3- pathway markedly reduced the survival of WT myocytes in the presence of ISO, but did not affect those of AC6(?N/?N) and AC6(-/-) myocytes, suggesting an important role of AC6 in mediating cardioprotective action through the activation of PKA-Src-STAT3-signaling. CONCLUSIONS: Collectively, AC6-N controls the anchorage of cardiac AC6 on the sarcolemmal membrane, which enables the coupling of AC6 with the pro-survival PKA-STAT3 pathway. Our findings may facilitate the development of novel therapies for heart failure. Twit Text FOAVip The type VI adenylyl cyclase protects cardiomyocytes from -adrenergic stress by a PKA/STAT3-dependent pathway ????J Biomed Sci http://www.kidney.de/pget.php?&tw=1&pmid=28870220 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28870220 #FOAvip English Wikipedia <ref>{{Cite pmid|28870220 }}</ref> The type VI adenylyl cyclase protects cardiomyocytes from ?-adrenergic stress by a PKA/STAT3-dependent pathway #MMPMID28870220 Wu YS ; Chen CC ; Chien CL ; Lai HL ; Jiang ST ; Chen YC ; Lai LP ; Hsiao WF ; Chen WP ; Chern Y J Biomed Sci 2017[Sep]; 24 (1 ): 68 PMID28870220 show ga BACKGROUND: The type VI adenylyl cyclase (AC6) is a main contributor of cAMP production in the heart. The amino acid (aa) sequence of AC6 is highly homologous to that of another major cardiac adenylyl cyclase, AC5, except for its N-terminus (AC6-N, aa 1-86). Activation of AC6, rather than AC5, produces cardioprotective effects against heart failure, while the underlying mechanism remains to be unveiled. Using an AC6-null (AC6(-/-)) mouse and a knockin mouse with AC6-N deletion (AC6 (?N/?N)), we aimed to investigate the cardioprotective mechanism of AC6 in the heart. METHODS: Western blot analysis and immunofluorescence staining were performed to determine the intracellular distribution of AC6, AC6-?N (a truncated AC6 lacking the first 86 amino acids), and STAT3 activation. Activities of AC6 and AC6-?N in the heart were assessed by cAMP assay. Apoptosis of cardiomyocytes were evaluated by the TUNEL assay and a propidium iodine-based survival assay. Fibrosis was examined by collagen staining. RESULTS: Immunofluorescence staining revealed that cardiac AC6 was mainly anchored on the sarcolemmal membranes, while AC6-?N was redistributed to the sarcoplasmic reticulum. AC6(?N/?N) and AC6(-/-) mice had more apoptotic myocytes and cardiac remodeling than WT mice in experimental models of isoproterenol (ISO)-induced myocardial injury. Adult cardiomyocytes isolated from AC6(?N/?N) or AC6(-/-) mice survived poorly after exposure to ISO, which produced no effect on WT cardiomyocytes under the condition tested. Importantly, ISO treatment induced cardiac STAT3 phosphorylation/activation in WT mice, but not in AC6(?N/?N) and AC6(-/-) mice. Pharmacological blockage of PKA-, Src-, or STAT3- pathway markedly reduced the survival of WT myocytes in the presence of ISO, but did not affect those of AC6(?N/?N) and AC6(-/-) myocytes, suggesting an important role of AC6 in mediating cardioprotective action through the activation of PKA-Src-STAT3-signaling. CONCLUSIONS: Collectively, AC6-N controls the anchorage of cardiac AC6 on the sarcolemmal membrane, which enables the coupling of AC6 with the pro-survival PKA-STAT3 pathway. Our findings may facilitate the development of novel therapies for heart failure. |*Signal Transduction [MESH] |Adenylyl Cyclases/*genetics/metabolism [MESH] |Animals [MESH] |Apoptosis/drug effects [MESH] |Heart Failure/metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Myocytes, Cardiac/*metabolism [MESH] |Protective Agents/metabolism [MESH]The type VI adenylyl cyclase protects cardiomyocytes from ?-adrenergic(epmc).pdf DeepDyve Pubget Overpricing