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10.1038/s41467-017-01629-7 http://scihub22266oqcxt.onion/10.1038/s41467-017-01629-7 C5684340!5684340 !29133788     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 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\29133788 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nat+Commun 2017 ; 8 (1 ): 1467 Nephropedia Template TP {{tp|p=29133788 |t=2017. Regulation of angiotensin II actions by enhancers and super-enhancers in vascular smooth muscle cells |pdf=|usr=}}{{29133788 }} gab.com Text Regulation of angiotensin II actions by enhancers and super-enhancers in vascular smooth muscle cells JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29133788 #FOAvip Angiotensin II (AngII) promotes hypertension and atherosclerosis by activating growth-promoting and pro-inflammatory gene expression in vascular smooth muscle cells (VSMCs). Enhancers and super-enhancers (SEs) play critical roles in driving disease-associated gene expression. However, enhancers/SEs mediating VSMC dysfunction remain uncharacterized. Here, we show that AngII alters vascular enhancer and SE repertoires in cultured VSMCs in vitro, ex vivo, and in AngII-infused mice aortas in vivo. AngII-induced enhancers/SEs are enriched in binding sites for signal-dependent transcription factors and dependent on key signaling kinases. Moreover, CRISPR-Cas9-mediated deletion of candidate enhancers/SEs, targeting SEs with the bromodomain and extra-terminal domain inhibitor JQ1, or knockdown of overlapping long noncoding RNAs (lncRNAs) blocks AngII-induced genes associated with growth-factor signaling and atherosclerosis. Furthermore, JQ1 ameliorates AngII-induced hypertension, medial hypertrophy and inflammation in vivo in mice. These results demonstrate AngII-induced signals integrate enhancers/SEs and lncRNAs to increase expression of genes involved in VSMC dysfunction, and could uncover novel therapies. Twit Text FOAVip Regulation of angiotensin II actions by enhancers and super-enhancers in vascular smooth muscle cells ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29133788 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29133788 #FOAvip English Wikipedia <ref>{{Cite pmid|29133788 }}</ref> Regulation of angiotensin II actions by enhancers and super-enhancers in vascular smooth muscle cells #MMPMID29133788 Das S ; Senapati P ; Chen Z ; Reddy MA ; Ganguly R ; Lanting L ; Mandi V ; Bansal A ; Leung A ; Zhang S ; Jia Y ; Wu X ; Schones DE ; Natarajan R Nat Commun 2017[Nov]; 8 (1 ): 1467 PMID29133788 show ga Angiotensin II (AngII) promotes hypertension and atherosclerosis by activating growth-promoting and pro-inflammatory gene expression in vascular smooth muscle cells (VSMCs). Enhancers and super-enhancers (SEs) play critical roles in driving disease-associated gene expression. However, enhancers/SEs mediating VSMC dysfunction remain uncharacterized. Here, we show that AngII alters vascular enhancer and SE repertoires in cultured VSMCs in vitro, ex vivo, and in AngII-infused mice aortas in vivo. AngII-induced enhancers/SEs are enriched in binding sites for signal-dependent transcription factors and dependent on key signaling kinases. Moreover, CRISPR-Cas9-mediated deletion of candidate enhancers/SEs, targeting SEs with the bromodomain and extra-terminal domain inhibitor JQ1, or knockdown of overlapping long noncoding RNAs (lncRNAs) blocks AngII-induced genes associated with growth-factor signaling and atherosclerosis. Furthermore, JQ1 ameliorates AngII-induced hypertension, medial hypertrophy and inflammation in vivo in mice. These results demonstrate AngII-induced signals integrate enhancers/SEs and lncRNAs to increase expression of genes involved in VSMC dysfunction, and could uncover novel therapies. |Angiotensin II/*metabolism [MESH] |Animals [MESH] |Aorta/cytology/pathology [MESH] |Atherosclerosis/drug therapy/*genetics [MESH] |Azepines/pharmacology [MESH] |Cells, Cultured [MESH] |Gene Expression Regulation [MESH] |Histones/metabolism [MESH] |Hypertension/drug therapy/*genetics [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Muscle, Smooth, Vascular/*pathology [MESH] |Myocytes, Smooth Muscle/*pathology [MESH] |RNA, Long Noncoding/*genetics [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Signal Transduction/genetics [MESH]Regulation of angiotensin II actions by enhancers and super-enhancers (epmc).pdf DeepDyve Pubget Overpricing