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10.1161/CIRCULATIONAHA.115.015687 http://scihub22266oqcxt.onion/10.1161/CIRCULATIONAHA.115.015687 C4470842!4470842!25995315     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       Circulation 2015 ; 131 (24): 2120-30 Nephropedia Template TP {{tp|p=25995315|t=2015. Circulating Exosomes Induced by Cardiac Pressure Overload Contain Functional Angiotensin II Type 1 Receptors |pdf=|usr=}}{{25995315}} gab.com Text Circulating Exosomes Induced by Cardiac Pressure Overload Contain Functional Angiotensin II Type 1 Receptors JO: Circulation http://www.kidney.de/pget.php?&tw=1&pmid=25995315 #FOAvip Background: Whether biomechanical force on the heart can induce exosome secretion to modulate cardiovascular function is not known. We investigated the secretion and activity of exosomes containing a key receptor in cardiovascular function, the Angiotensin II Type I Receptor (AT1R). Methods and Results: Exosomes containing AT1Rs were isolated from the media overlying AT1R-overexpressing cells exposed to osmotic stretch and from sera of mice undergoing cardiac pressure overload. The presence of AT1Rs in exosomes was confirmed by both electron microscopy and radioligand receptor binding assays, and shown to require ?-arrestin2, a multifunctional adaptor protein essential for receptor trafficking. We show that functional AT1Rs are transferred via exosomes in an in vitro model of cellular stretch. Using mice with global and cardiomyocyte conditional deletion of ?-arrestin2, we show that under conditions of in vivo pressure overload the cellular source for the exocytosis of exosomes containing AT1R is the cardiomyocyte. Exogenous administered AT1R-enriched exosomes target cardiomyocytes, skeletal myocytes and mesenteric resistance vessels, and is sufficient to confer blood pressure responsiveness to angiotensin II infusion in AT1R knockout mice. Conclusions: This work reveals that AT1R-enriched exosomes are released from the heart under conditions of in vivo cellular stress to likely modulate vascular responses to neurohormonal stimulation. In the context of the whole organism, the concept of G protein-coupled receptor trafficking should consider circulating exosomes as part of the reservoir of functional AT1Rs. Twit Text FOAVip Circulating Exosomes Induced by Cardiac Pressure Overload Contain Functional Angiotensin II Type 1 Receptors ????Circulation http://www.kidney.de/pget.php?&tw=1&pmid=25995315 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25995315 #FOAvip English Wikipedia <ref>{{Cite pmid|25995315}}</ref> Circulating Exosomes Induced by Cardiac Pressure Overload Contain Functional Angiotensin II Type 1 Receptors #MMPMID25995315 Pironti G; Strachan RT; Abraham D; Yu SMW; Chen M; Chen W; Hanada K; Mao L; Watson LJ; Rockman HA Circulation 2015[Jun]; 131 (24): 2120-30 PMID25995315show ga Background: Whether biomechanical force on the heart can induce exosome secretion to modulate cardiovascular function is not known. We investigated the secretion and activity of exosomes containing a key receptor in cardiovascular function, the Angiotensin II Type I Receptor (AT1R). Methods and Results: Exosomes containing AT1Rs were isolated from the media overlying AT1R-overexpressing cells exposed to osmotic stretch and from sera of mice undergoing cardiac pressure overload. The presence of AT1Rs in exosomes was confirmed by both electron microscopy and radioligand receptor binding assays, and shown to require ?-arrestin2, a multifunctional adaptor protein essential for receptor trafficking. We show that functional AT1Rs are transferred via exosomes in an in vitro model of cellular stretch. Using mice with global and cardiomyocyte conditional deletion of ?-arrestin2, we show that under conditions of in vivo pressure overload the cellular source for the exocytosis of exosomes containing AT1R is the cardiomyocyte. Exogenous administered AT1R-enriched exosomes target cardiomyocytes, skeletal myocytes and mesenteric resistance vessels, and is sufficient to confer blood pressure responsiveness to angiotensin II infusion in AT1R knockout mice. Conclusions: This work reveals that AT1R-enriched exosomes are released from the heart under conditions of in vivo cellular stress to likely modulate vascular responses to neurohormonal stimulation. In the context of the whole organism, the concept of G protein-coupled receptor trafficking should consider circulating exosomes as part of the reservoir of functional AT1Rs. äCirculating Exosomes Induced by Cardiac Pressure Overload Contain Func(epmc).pdf DeepDyve Pubget Overpricing