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10.1038/ncomms7725 http://scihub22266oqcxt.onion/10.1038/ncomms7725 C4394241!4394241!25857352     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2015 ; 6 (ä): 6725 Nephropedia Template TP {{tp|p=25857352|t=2015. RhoA and ROCK mediate histamine-induced vascular leakage and anaphylactic shock |pdf=|usr=}}{{25857352}} gab.com Text RhoA and ROCK mediate histamine-induced vascular leakage and anaphylactic shock JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25857352 #FOAvip Histamine-induced vascular leakage is an integral component of many highly prevalent human diseases, including allergies, asthma, and anaphylaxis. Yet, how histamine induces the disruption of the endothelial barrier is not well defined. By using genetically modified animal models, pharmacologic inhibitors, and a synthetic biology approach, here we show that the small GTPase RhoA mediates histamine-induced vascular leakage. Histamine causes the rapid formation of focal adherens junctions, disrupting the endothelial barrier by acting on H1R G?q-coupled receptors, which is blunted in endothelial G?q/11 KO mice. Interfering with RhoA and ROCK function abolishes endothelial permeability, while phospholipase C? plays a limited role. Moreover, endothelial-specific RhoA gene deletion prevents vascular leakage and passive cutaneous anaphylaxis in vivo, and ROCK inhibitors protect from lethal systemic anaphylaxis. This study supports a key role for the RhoA signaling circuitry in vascular permeability, thereby identifying novel pharmacological targets for many human diseases characterized by aberrant vascular leakage. Twit Text FOAVip RhoA and ROCK mediate histamine-induced vascular leakage and anaphylactic shock ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25857352 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25857352 #FOAvip English Wikipedia <ref>{{Cite pmid|25857352}}</ref> RhoA and ROCK mediate histamine-induced vascular leakage and anaphylactic shock #MMPMID25857352 Mikelis CM; Simaan M; Ando K; Fukuhara S; Sakurai A; Amornphimoltham P; Masedunskas A; Weigert R; Chavakis T; Adams R; Offermanns S; Mochizuki N; Zheng Y; Gutkind JS Nat Commun 2015[]; 6 (ä): 6725 PMID25857352show ga Histamine-induced vascular leakage is an integral component of many highly prevalent human diseases, including allergies, asthma, and anaphylaxis. Yet, how histamine induces the disruption of the endothelial barrier is not well defined. By using genetically modified animal models, pharmacologic inhibitors, and a synthetic biology approach, here we show that the small GTPase RhoA mediates histamine-induced vascular leakage. Histamine causes the rapid formation of focal adherens junctions, disrupting the endothelial barrier by acting on H1R G?q-coupled receptors, which is blunted in endothelial G?q/11 KO mice. Interfering with RhoA and ROCK function abolishes endothelial permeability, while phospholipase C? plays a limited role. Moreover, endothelial-specific RhoA gene deletion prevents vascular leakage and passive cutaneous anaphylaxis in vivo, and ROCK inhibitors protect from lethal systemic anaphylaxis. This study supports a key role for the RhoA signaling circuitry in vascular permeability, thereby identifying novel pharmacological targets for many human diseases characterized by aberrant vascular leakage. äRhoA and ROCK mediate histamine-induced vascular leakage and anaphylac(epmc).pdf DeepDyve Pubget Overpricing