The heme oxygenase-1/carbon monoxide pathway suppresses TLR4 signaling by regulating the interaction of TLR4 with caveolin-1.
作者： Xiao Mei Wang , Hong Pyo Kim , Kiichi Nakahira , Stefan W. Ryter , Augustine M. K. Choi
关键词:
摘要: Caveolin-1 (cav-1), the principle structural protein of plasmalemmal caveolae, regulates inflammatory signaling processes originating at membrane. We show that cav-1 bound to TLR4 and inhibited LPS-induced proinflammatory cytokine (TNF-α IL-6) production in murine macrophages. Mutation analysis revealed a binding motif TLR4, essential for this interaction attenuation signaling. Cav-1 was required anti-inflammatory effects carbon monoxide (CO), product heme oxygenase-1 (HO-1) activity. CO augmented cav-1/TLR4 interaction. Upon LPS stimulation, HO-1 trafficked caveolae by p38 MAPK-dependent mechanism, where it down-regulated These results reveal an network involving HO-1.
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