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10.1111/bph.13657 http://scihub22266oqcxt.onion/10.1111/bph.13657 27774624!5341496!27774624     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Br+J+Pharmacol 2017 ; 174 (1): 101-115 Nephropedia Template TP {{tp|p=27774624|t=2017. The suppression of bromodomain and extra-terminal domain inhibits vascular inflammation by blocking NF-kappaB and MAPK activation |pdf=|usr=}}{{27774624}} gab.com Text The suppression of bromodomain and extra-terminal domain inhibits vascular inflammation by blocking NF-kappaB and MAPK activation JO: Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=27774624 #FOAvip BACKGROUND AND PURPOSE: There is increasing evidence indicating that bromodomain and extra-terminal domain (BET) proteins play a critical role in the regulation of immune and inflammatory responses; however, their contribution to vascular inflammation has not yet been elucidated. In this study, we investigated the effect of inhibiting BET bromodomain on vascular inflammation and the underlying mechanisms. EXPERIMENTAL APPROACH: HUVECs were isolated from fresh umbilical cords. JQ1, a specific BET bromodomain inhibitor, and Brd shRNA were used to evaluate the regulation of the BET proteins in vascular inflammation. Leukocyte adhesion to HUVECs was measure by an adhesion assay. Western blot or immunohistochemical analysis was used to detect the protein expression. Real-time PCR was used to evaluate mRNA expression. Leukocyte accumulation in vivo was determined by an acute lung inflammation model. KEY RESULTS: BET bromodomain inhibition suppressed the expression of adhesion molecules induced by TNF-alpha- or LPS, including ICAM-1, VCAM-1 and E-selectin, and inhibited leukocyte adhesion to activated HUVEC monolayers. Treatment with JQ1 also attenuated the LPS-induced accumulation of leukocytes and expression of endothelial adhesion molecules in the acute lung inflammation model in vivo. Furthermore, BET bromodomain inhibition reduced the activity of p38 and JNK MAPKs and NF-kappaB in TNF-alpha-stimulated HUVECs. TNF-alpha-induced NF-kappaB activation was also blocked by inhibitors of p38 (SB203580) or JNK (SP600125). CONCLUSIONS AND IMPLICATIONS: BET bromodomain is important for regulating endothelial inflammation. Strategies targeting endothelial BET bromodomain may provide a new therapeutic approach for controlling inflammatory-related diseases. Twit Text FOAVip The suppression of bromodomain and extra-terminal domain inhibits vascular inflammation by blocking NF-kappaB and MAPK activation ????Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=27774624 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27774624 #FOAvip English Wikipedia <ref>{{Cite pmid|27774624}}</ref> The suppression of bromodomain and extra-terminal domain inhibits vascular inflammation by blocking NF-kappaB and MAPK activation #MMPMID27774624 Huang M; Zeng S; Zou Y; Shi M; Qiu Q; Xiao Y; Chen G; Yang X; Liang L; Xu H Br J Pharmacol 2017[Jan]; 174 (1): 101-115 PMID27774624show ga BACKGROUND AND PURPOSE: There is increasing evidence indicating that bromodomain and extra-terminal domain (BET) proteins play a critical role in the regulation of immune and inflammatory responses; however, their contribution to vascular inflammation has not yet been elucidated. In this study, we investigated the effect of inhibiting BET bromodomain on vascular inflammation and the underlying mechanisms. EXPERIMENTAL APPROACH: HUVECs were isolated from fresh umbilical cords. JQ1, a specific BET bromodomain inhibitor, and Brd shRNA were used to evaluate the regulation of the BET proteins in vascular inflammation. Leukocyte adhesion to HUVECs was measure by an adhesion assay. Western blot or immunohistochemical analysis was used to detect the protein expression. Real-time PCR was used to evaluate mRNA expression. Leukocyte accumulation in vivo was determined by an acute lung inflammation model. KEY RESULTS: BET bromodomain inhibition suppressed the expression of adhesion molecules induced by TNF-alpha- or LPS, including ICAM-1, VCAM-1 and E-selectin, and inhibited leukocyte adhesion to activated HUVEC monolayers. Treatment with JQ1 also attenuated the LPS-induced accumulation of leukocytes and expression of endothelial adhesion molecules in the acute lung inflammation model in vivo. Furthermore, BET bromodomain inhibition reduced the activity of p38 and JNK MAPKs and NF-kappaB in TNF-alpha-stimulated HUVECs. TNF-alpha-induced NF-kappaB activation was also blocked by inhibitors of p38 (SB203580) or JNK (SP600125). CONCLUSIONS AND IMPLICATIONS: BET bromodomain is important for regulating endothelial inflammation. Strategies targeting endothelial BET bromodomain may provide a new therapeutic approach for controlling inflammatory-related diseases. |Azepines/*pharmacology[MESH] |Cells, Cultured[MESH] |Dose-Response Relationship, Drug[MESH] |Enzyme Activation/drug effects[MESH] |Humans[MESH] |Inflammation/*drug therapy/metabolism[MESH] |Mitogen-Activated Protein Kinases/*metabolism[MESH] |NF-kappa B/*metabolism[MESH] |Protein Kinase Inhibitors/*pharmacology[MESH] |Structure-Activity Relationship[MESH] |Transcription Factors/*antagonists & inhibitors/*metabolism[MESH]The suppression of bromodomain and extra-terminal domain inhibits vasc(epmc).pdf DeepDyve Pubget Overpricing