A novel mechanism involved in TLR4 expression during inflammation.
The p47phox- and Rac 1-dependent NADPH oxidase activation, ROS production, and MAPK signaling pathways play critical roles in endotoxin-enhanced TLR4 expression and TLR4 mRNA stabilization in VSMCs. These evidences provide for the direct involvement of VSMCs in endotoxin-mediated inflammatory activation, which may contribute to the progression of cardiovascular disorders, although targeting TLR4 will prove to be a successful approach for the treatment of these devastating diseases remains to be determined.
Li
Chi-Yuan
CY
Lin
Feng-Yen
FY
D000818:Animals; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism; D019255:NADPH Oxidases / Q000502:physiology; D012333:RNA, Messenger / Q000032:analysis; D051197:Toll-Like Receptor 4 / Q000235:genetics*; D048051:p38 Mitogen-Activated Protein Kinases / Q000502:physiology
D012333:RNA, Messenger; D051197:Toll-Like Receptor 4; D019255:NADPH Oxidases; D048051:p38 Mitogen-Activated Protein Kinases