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10.1152/ajprenal.00547.2016 http://scihub22266oqcxt.onion/10.1152/ajprenal.00547.2016 C5407068!5407068!28100502     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2017 ; 312 (4): F565-76 Nephropedia Template TP {{tp|p=28100502|t=2017. RACK1 regulates angiotensin II-induced contractions of SHR preglomerular vascular smooth muscle cells |pdf=|usr=}}{{28100502}} gab.com Text RACK1 regulates angiotensin II-induced contractions of SHR preglomerular vascular smooth muscle cells JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28100502 #FOAvip The preglomerular microcirculation of spontaneously hypertensive rats (SHR) is hypersensitive to angiotensin (ANG) II, and studies have shown that this is likely due to enhanced coincident signaling between G protein subunits ?q (G?q; released by ANG II) and ?? (G??; released by Gi-coupled receptors) to active phospholipase C (PLC). Here we investigated the molecular basis for the enhanced coincident signaling between G?? and G?q in SHR preglomerular vascular smooth muscle cells (PGVSMCs). Because receptor for activated C kinase 1 (RACK1; a scaffolding protein) organizes interactions between G??, G?q, and PLC, we included RACK1 in this investigation. Cell fractionation studies demonstrated increased levels of membrane (but not cytosolic) G?, G?q, PLC?3, and RACK1 in SHR PGVSMCs compared with Wistar-Kyoto rat PGVSMCs. In SHR PGVSMCs, coimmunoprecipitation demonstrated RACK1 binding to G? and PLC?3, but only at cell membranes. Pertussis toxin (which blocks G??) and U73122 (which blocks PLC) reduced membrane RACK1; however, RACK1 knockdown (shRNA) did not affect membrane levels of G?, G?q, or PLC?3. In a novel gel contraction assay, RACK1 knockdown in SHR PGVSMCs attenuated contractions to ANG II and abrogated the ability of neuropeptide Y (which signals via G??) to enhance ANG II-induced contractions. We conclude that in SHR PGVSMCs the enlarged pool of G?? and PLC?3 recruits RACK1 to membranes and RACK1 then organizes signaling. Consequently, knockdown of RACK1 prevents coincident signaling between ANG II and the Gi pathway. This is the first study to implicate RACK1 in vascular smooth muscle cell contraction and suggests that RACK1 inhibitors could be effective cardiovascular drugs. Twit Text FOAVip RACK1 regulates angiotensin II-induced contractions of SHR preglomerular vascular smooth muscle cells ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=28100502 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28100502 #FOAvip English Wikipedia <ref>{{Cite pmid|28100502}}</ref> RACK1 regulates angiotensin II-induced contractions of SHR preglomerular vascular smooth muscle cells #MMPMID28100502 Zhu X; Jackson EK Am J Physiol Renal Physiol 2017[Apr]; 312 (4): F565-76 PMID28100502show ga The preglomerular microcirculation of spontaneously hypertensive rats (SHR) is hypersensitive to angiotensin (ANG) II, and studies have shown that this is likely due to enhanced coincident signaling between G protein subunits ?q (G?q; released by ANG II) and ?? (G??; released by Gi-coupled receptors) to active phospholipase C (PLC). Here we investigated the molecular basis for the enhanced coincident signaling between G?? and G?q in SHR preglomerular vascular smooth muscle cells (PGVSMCs). Because receptor for activated C kinase 1 (RACK1; a scaffolding protein) organizes interactions between G??, G?q, and PLC, we included RACK1 in this investigation. Cell fractionation studies demonstrated increased levels of membrane (but not cytosolic) G?, G?q, PLC?3, and RACK1 in SHR PGVSMCs compared with Wistar-Kyoto rat PGVSMCs. In SHR PGVSMCs, coimmunoprecipitation demonstrated RACK1 binding to G? and PLC?3, but only at cell membranes. Pertussis toxin (which blocks G??) and U73122 (which blocks PLC) reduced membrane RACK1; however, RACK1 knockdown (shRNA) did not affect membrane levels of G?, G?q, or PLC?3. In a novel gel contraction assay, RACK1 knockdown in SHR PGVSMCs attenuated contractions to ANG II and abrogated the ability of neuropeptide Y (which signals via G??) to enhance ANG II-induced contractions. We conclude that in SHR PGVSMCs the enlarged pool of G?? and PLC?3 recruits RACK1 to membranes and RACK1 then organizes signaling. Consequently, knockdown of RACK1 prevents coincident signaling between ANG II and the Gi pathway. This is the first study to implicate RACK1 in vascular smooth muscle cell contraction and suggests that RACK1 inhibitors could be effective cardiovascular drugs. äRACK1 regulates angiotensin II-induced contractions of SHR preglomerul(epmc).pdf DeepDyve Pubget Overpricing