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10.1152/ajpcell.00235.2012 http://scihub22266oqcxt.onion/10.1152/ajpcell.00235.2012 C3680646!3680646 !23576578     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 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\23576578 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Physiol+Cell+Physiol 2013 ; 304 (12 ): C1176-86 Nephropedia Template TP {{tp|p=23576578 |t=2013. Angiotensin II activates NF-?B through AT1A receptor recruitment of ?-arrestin in cultured rat vascular smooth muscle cells |pdf=|usr=}}{{23576578 }} gab.com Text Angiotensin II activates NF- B through AT1A receptor recruitment of -arrestin in cultured rat vascular smooth muscle cells JO: Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=23576578 #FOAvip Activation of the angiotensin type 1A receptor (AT1AR) in rat aorta vascular smooth muscle cells (RASMC) results in increased synthesis of the proinflammatory enzyme cyclooxygenase-2 (COX-2). We previously showed that nuclear localization of internalized AT1AR results in activation of transcription of the gene for COX-2, i.e., prostaglandin-endoperoxide synthase-2. Others have suggested that ANG II stimulation of COX-2 protein synthesis is mediated by NF-?B. The purpose of the present study was to examine the interrelationship between AT1AR activation, ?-arrestin recruitment, and NF-?B activation in the ability of ANG II to increase COX-2 protein synthesis in RASMC. In the present study we utilized RASMC, inhibitors of the NF-?B pathway, ?-arrestin knockdown, radioligand binding, immunoblotting, and immunofluorescence to characterize the roles of AT1AR internalization, NF-?B activation, and ?-arrestin in ANG II-induced COX-2 synthesis. Ro-106-9920 or parthenolide, agents that inhibit the initial steps of NF-?B activation, blocked ANG II-induced p65 NF-?B nuclear localization, COX-2 protein expression, ?-arrestin recruitment, and AT1AR internalization without inhibiting ANG II-induced p42/44 ERK activation. Curcumin, an inhibitor of NF-?B-induced transcription, blocked ANG II-induced COX-2 protein expression without altering AT1AR internalization, ANG II-induced p65 NF-?B nuclear localization, or p42/44 ERK activation. Small interfering RNA-induced knockdown of ?-arrestin-1 and -2 inhibited ANG II-induced p65 NF-?B nuclear localization. In vascular smooth muscle cells, internalization of the activated AT1AR mediated by ?-arrestins activates the NF-?B pathway, producing nuclear localization of the transcription factor and initiation of COX-2 protein synthesis, thereby linking internalization of the receptor with the NF-?B pathway. Twit Text FOAVip Angiotensin II activates NF- B through AT1A receptor recruitment of -arrestin in cultured rat vascular smooth muscle cells ????Am J Physiol Cell Physiol http://www.kidney.de/pget.php?&tw=1&pmid=23576578 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23576578 #FOAvip English Wikipedia <ref>{{Cite pmid|23576578 }}</ref> Angiotensin II activates NF-?B through AT1A receptor recruitment of ?-arrestin in cultured rat vascular smooth muscle cells #MMPMID23576578 Morinelli TA ; Lee MH ; Kendall RT ; Luttrell LM ; Walker LP ; Ullian ME Am J Physiol Cell Physiol 2013[Jun]; 304 (12 ): C1176-86 PMID23576578 show ga Activation of the angiotensin type 1A receptor (AT1AR) in rat aorta vascular smooth muscle cells (RASMC) results in increased synthesis of the proinflammatory enzyme cyclooxygenase-2 (COX-2). We previously showed that nuclear localization of internalized AT1AR results in activation of transcription of the gene for COX-2, i.e., prostaglandin-endoperoxide synthase-2. Others have suggested that ANG II stimulation of COX-2 protein synthesis is mediated by NF-?B. The purpose of the present study was to examine the interrelationship between AT1AR activation, ?-arrestin recruitment, and NF-?B activation in the ability of ANG II to increase COX-2 protein synthesis in RASMC. In the present study we utilized RASMC, inhibitors of the NF-?B pathway, ?-arrestin knockdown, radioligand binding, immunoblotting, and immunofluorescence to characterize the roles of AT1AR internalization, NF-?B activation, and ?-arrestin in ANG II-induced COX-2 synthesis. Ro-106-9920 or parthenolide, agents that inhibit the initial steps of NF-?B activation, blocked ANG II-induced p65 NF-?B nuclear localization, COX-2 protein expression, ?-arrestin recruitment, and AT1AR internalization without inhibiting ANG II-induced p42/44 ERK activation. Curcumin, an inhibitor of NF-?B-induced transcription, blocked ANG II-induced COX-2 protein expression without altering AT1AR internalization, ANG II-induced p65 NF-?B nuclear localization, or p42/44 ERK activation. Small interfering RNA-induced knockdown of ?-arrestin-1 and -2 inhibited ANG II-induced p65 NF-?B nuclear localization. In vascular smooth muscle cells, internalization of the activated AT1AR mediated by ?-arrestins activates the NF-?B pathway, producing nuclear localization of the transcription factor and initiation of COX-2 protein synthesis, thereby linking internalization of the receptor with the NF-?B pathway. |Angiotensin II/*pharmacology/physiology [MESH] |Animals [MESH] |Aorta, Thoracic/drug effects/metabolism [MESH] |Arrestins/*metabolism [MESH] |Cells, Cultured [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Male [MESH] |Muscle, Smooth, Vascular/drug effects/*metabolism [MESH] |Myocytes, Smooth Muscle/drug effects/*metabolism [MESH] |NF-kappa B/*metabolism [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Receptor, Angiotensin, Type 1/*metabolism [MESH] |beta-Arrestin 1 [MESH]Angiotensin II activates NF-?B through AT1A receptor recruitment of ?-(epmc).pdf DeepDyve Pubget Overpricing