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10.1016/j.jaci.2015.11.024 http://scihub22266oqcxt.onion/10.1016/j.jaci.2015.11.024 C4931983!4931983!26948077     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       J+Allergy+Clin+Immunol 2016 ; 138 (1): 187-99 Nephropedia Template TP {{tp|p=26948077|t=2016. Diminution of STAT3 signaling inhibits vascular permeability and anaphylaxis |pdf=|usr=}}{{26948077}} gab.com Text Diminution of STAT3 signaling inhibits vascular permeability and anaphylaxis JO: J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26948077 #FOAvip Background: During IgE-mediated immediate hypersensitivity reactions, vascular endothelial cells permeabilize in response to mast cell mediators. We have previously demonstrated that patients and mice with STAT3 mutations (autosomal dominant-hyper IgE syndrome; AD-HIES) are partially protected from anaphylaxis. Objectives: To further study the mechanism by which STAT3 contributes to anaphylaxis, and determine whether small molecule inhibition of STAT3 can prevent anaphylaxis. Methods: Using unaffected and STAT3-inhibited or genetic loss of function samples, we performed histamine skin prick testing, investigated the contribution of STAT3 to animal models of anaphylaxis, measured endothelial cell permeability, gene and protein expression, and histamine receptor-mediated signaling. Results: While mouse mast cell degranulation was minimally affected by STAT3 blockade, mast cell mediator-induced anaphylaxis was blunted in Stat3 mutant AD-HIES mice and in wild-type mice subjected to small molecule STAT3 inhibition. Histamine skin prick responses were diminished in AD-HIES patients. Human umbilical vein vascular endothelial cells (HUVECs) derived from patients with AD-HIES or treated with a STAT3 inhibitor failed to properly signal through Src or to appropriately dissolute the adherens junctions made up of the proteins vascular endothelial (VE)-cadherin and ?-catenin. Further, we found that diminished STAT3-target mir17?92 expression in AD-HIES HUVECS is associated with increased PTEN expression, which inhibits Src, and increased E2F1 expression, which regulates ?-catenin cellular dynamics. Conclusions: These data demonstrate that STAT3-dependent transcriptional activity regulates critical components for the architecture and functional dynamics of endothelial junctions thus permitting vascular permeability. Twit Text FOAVip Diminution of STAT3 signaling inhibits vascular permeability and anaphylaxis ????J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26948077 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26948077 #FOAvip English Wikipedia <ref>{{Cite pmid|26948077}}</ref> Diminution of STAT3 signaling inhibits vascular permeability and anaphylaxis #MMPMID26948077 Hox V; O?Connell MP; Lyons JJ; Sackstein P; Dimaggio T; Jones N; Nelson C; Boehm M; Holland SM; Freeman AF; Tweardy DJ; Olivera A; Metcalfe DD; Milner JD J Allergy Clin Immunol 2016[Jul]; 138 (1): 187-99 PMID26948077show ga Background: During IgE-mediated immediate hypersensitivity reactions, vascular endothelial cells permeabilize in response to mast cell mediators. We have previously demonstrated that patients and mice with STAT3 mutations (autosomal dominant-hyper IgE syndrome; AD-HIES) are partially protected from anaphylaxis. Objectives: To further study the mechanism by which STAT3 contributes to anaphylaxis, and determine whether small molecule inhibition of STAT3 can prevent anaphylaxis. Methods: Using unaffected and STAT3-inhibited or genetic loss of function samples, we performed histamine skin prick testing, investigated the contribution of STAT3 to animal models of anaphylaxis, measured endothelial cell permeability, gene and protein expression, and histamine receptor-mediated signaling. Results: While mouse mast cell degranulation was minimally affected by STAT3 blockade, mast cell mediator-induced anaphylaxis was blunted in Stat3 mutant AD-HIES mice and in wild-type mice subjected to small molecule STAT3 inhibition. Histamine skin prick responses were diminished in AD-HIES patients. Human umbilical vein vascular endothelial cells (HUVECs) derived from patients with AD-HIES or treated with a STAT3 inhibitor failed to properly signal through Src or to appropriately dissolute the adherens junctions made up of the proteins vascular endothelial (VE)-cadherin and ?-catenin. Further, we found that diminished STAT3-target mir17?92 expression in AD-HIES HUVECS is associated with increased PTEN expression, which inhibits Src, and increased E2F1 expression, which regulates ?-catenin cellular dynamics. Conclusions: These data demonstrate that STAT3-dependent transcriptional activity regulates critical components for the architecture and functional dynamics of endothelial junctions thus permitting vascular permeability. äDiminution of STAT3 signaling inhibits vascular permeability and anaph(epmc).pdf DeepDyve Pubget Overpricing