Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1161/JAHA.116.003336 http://scihub22266oqcxt.onion/10.1161/JAHA.116.003336 C4859298!4859298!27048969     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Heart+Assoc 2016 ; 5 (4): ä Nephropedia Template TP {{tp|p=27048969|t=2016. Rnd3 as a Novel Target to Ameliorate Microvascular Leakage |pdf=|usr=}}{{27048969}} gab.com Text Rnd3 as a Novel Target to Ameliorate Microvascular Leakage JO: J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=27048969 #FOAvip Background: Microvascular leakage of plasma proteins is a hallmark of inflammation that leads to tissue dysfunction. There are no current therapeutic strategies to reduce microvascular permeability. The purpose of this study was to identify the role of Rnd3, an atypical Rho family GTPase, in the control of endothelial barrier integrity. The potential therapeutic benefit of Rnd3 protein delivery to ameliorate microvascular leakage was also investigated. Methods and Results: Using immunofluorescence microscopy, Rnd3 was observed primarily in cytoplasmic areas around the nuclei of human umbilical vein endothelial cells. Permeability to fluorescein isothiocyanate?albumin and transendothelial electrical resistance of human umbilical vein endothelial cell monolayers served as indices of barrier function, and RhoA, Rac1, and Cdc42 activities were determined using G?LISA assays. Overexpression of Rnd3 significantly reduced the magnitude of thrombin?induced barrier dysfunction, and abolished thrombin?induced Rac1 inactivation. Depleting Rnd3 expression with siRNA significantly extended the time course of thrombin?induced barrier dysfunction and Rac1 inactivation. Time?lapse microscopy of human umbilical vein endothelial cells expressing GFP?actin showed that co?expression of mCherry?Rnd3 attenuated thrombin?induced reductions in local lamellipodia that accompany endothelial barrier dysfunction. Lastly, a novel Rnd3 protein delivery method reduced microvascular leakage in a rat model of hemorrhagic shock and resuscitation, assessed by both intravital microscopic observation of extravasation of fluorescein isothiocyanate?albumin from the mesenteric microcirculation, and direct determination of solute permeability in intact isolated venules. Conclusions: The data suggest that Rnd3 can shift the balance of RhoA and Rac1 signaling in endothelial cells. In addition, our findings suggest the therapeutic, anti?inflammatory potential of delivering Rnd3 to promote endothelial barrier recovery during inflammatory challenge. Twit Text FOAVip Rnd3 as a Novel Target to Ameliorate Microvascular Leakage ????J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=27048969 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27048969 #FOAvip English Wikipedia <ref>{{Cite pmid|27048969}}</ref> Rnd3 as a Novel Target to Ameliorate Microvascular Leakage #MMPMID27048969 Breslin JW; Daines DA; Doggett TM; Kurtz KH; Souza?Smith FM; Zhang XE; Wu MH; Yuan SY J Am Heart Assoc 2016[Apr]; 5 (4): ä PMID27048969show ga Background: Microvascular leakage of plasma proteins is a hallmark of inflammation that leads to tissue dysfunction. There are no current therapeutic strategies to reduce microvascular permeability. The purpose of this study was to identify the role of Rnd3, an atypical Rho family GTPase, in the control of endothelial barrier integrity. The potential therapeutic benefit of Rnd3 protein delivery to ameliorate microvascular leakage was also investigated. Methods and Results: Using immunofluorescence microscopy, Rnd3 was observed primarily in cytoplasmic areas around the nuclei of human umbilical vein endothelial cells. Permeability to fluorescein isothiocyanate?albumin and transendothelial electrical resistance of human umbilical vein endothelial cell monolayers served as indices of barrier function, and RhoA, Rac1, and Cdc42 activities were determined using G?LISA assays. Overexpression of Rnd3 significantly reduced the magnitude of thrombin?induced barrier dysfunction, and abolished thrombin?induced Rac1 inactivation. Depleting Rnd3 expression with siRNA significantly extended the time course of thrombin?induced barrier dysfunction and Rac1 inactivation. Time?lapse microscopy of human umbilical vein endothelial cells expressing GFP?actin showed that co?expression of mCherry?Rnd3 attenuated thrombin?induced reductions in local lamellipodia that accompany endothelial barrier dysfunction. Lastly, a novel Rnd3 protein delivery method reduced microvascular leakage in a rat model of hemorrhagic shock and resuscitation, assessed by both intravital microscopic observation of extravasation of fluorescein isothiocyanate?albumin from the mesenteric microcirculation, and direct determination of solute permeability in intact isolated venules. Conclusions: The data suggest that Rnd3 can shift the balance of RhoA and Rac1 signaling in endothelial cells. In addition, our findings suggest the therapeutic, anti?inflammatory potential of delivering Rnd3 to promote endothelial barrier recovery during inflammatory challenge. äRnd3 as a Novel Target to Ameliorate Microvascular Leakage (epmc).pdf DeepDyve Pubget Overpricing