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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 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 Deprecated: Implicit conversion from float 265.2 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26948077 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Allergy+Clin+Immunol 2016 ; 138 (1 ): 187-199 Nephropedia Template TP {{tp|p=26948077 |t=2016. Diminution of signal transducer and activator of transcription 3 signaling inhibits vascular permeability and anaphylaxis |pdf=|usr=}}{{26948077 }} gab.com Text Diminution of signal transducer and activator of transcription 3 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 demonstrated previously that patients and mice with signal transducer and activator of transcription 3 (STAT3) mutations (autosomal dominant hyper-IgE syndrome [AD-HIES]) are partially protected from anaphylaxis. OBJECTIVES: We sought to 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 tests, investigated the contribution of STAT3 to animal models of anaphylaxis, and measured endothelial cell permeability, gene and protein expression, and histamine receptor-mediated signaling. RESULTS: Although mouse mast cell degranulation was minimally affected by STAT3 blockade, mast cell mediator-induced anaphylaxis was blunted in Stat3 mutant mice with AD-HIES and in wild-type mice subjected to small-molecule STAT3 inhibition. Histamine skin prick test responses were diminished in patients with AD-HIES. Human umbilical vein endothelial cells derived from patients with AD-HIES or treated with a STAT3 inhibitor did not signal properly through Src or cause appropriate dissolution of the adherens junctions made up of the proteins vascular endothelial-cadherin and ?-catenin. Furthermore, we found that diminished STAT3 target microRNA17-92 expression in human umbilical vein endothelial cells from patients with AD-HIES is associated with increased phosphatase and tensin homolog (PTEN) expression, which inhibits Src, and increased E2F transcription factor 1 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 signal transducer and activator of transcription 3 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 signal transducer and activator of transcription 3 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 ): 187-199 PMID26948077 show ga BACKGROUND: During IgE-mediated immediate hypersensitivity reactions, vascular endothelial cells permeabilize in response to mast cell mediators. We have demonstrated previously that patients and mice with signal transducer and activator of transcription 3 (STAT3) mutations (autosomal dominant hyper-IgE syndrome [AD-HIES]) are partially protected from anaphylaxis. OBJECTIVES: We sought to 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 tests, investigated the contribution of STAT3 to animal models of anaphylaxis, and measured endothelial cell permeability, gene and protein expression, and histamine receptor-mediated signaling. RESULTS: Although mouse mast cell degranulation was minimally affected by STAT3 blockade, mast cell mediator-induced anaphylaxis was blunted in Stat3 mutant mice with AD-HIES and in wild-type mice subjected to small-molecule STAT3 inhibition. Histamine skin prick test responses were diminished in patients with AD-HIES. Human umbilical vein endothelial cells derived from patients with AD-HIES or treated with a STAT3 inhibitor did not signal properly through Src or cause appropriate dissolution of the adherens junctions made up of the proteins vascular endothelial-cadherin and ?-catenin. Furthermore, we found that diminished STAT3 target microRNA17-92 expression in human umbilical vein endothelial cells from patients with AD-HIES is associated with increased phosphatase and tensin homolog (PTEN) expression, which inhibits Src, and increased E2F transcription factor 1 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. |*Signal Transduction/drug effects [MESH] |Adherens Junctions/metabolism [MESH] |Anaphylaxis/diagnosis/genetics/*immunology/*metabolism [MESH] |Animals [MESH] |Capillary Permeability/drug effects/genetics/*immunology [MESH] |Cell Degranulation/drug effects/immunology [MESH] |Cytokines/metabolism [MESH] |Disease Models, Animal [MESH] |Human Umbilical Vein Endothelial Cells [MESH] |Humans [MESH] |Immunoglobulin E/immunology [MESH] |Inflammation Mediators/metabolism [MESH] |Mast Cells/metabolism [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Mutation [MESH] |Receptors, Histamine/immunology/metabolism [MESH] |STAT3 Transcription Factor/antagonists & inhibitors/genetics/*metabolism [MESH] |Skin Tests [MESH] |beta Catenin/metabolism [MESH]Diminution of signal transducer and activator of transcription 3 signa(epmc).pdf DeepDyve Pubget Overpricing