Advanced oxidation protein products induce chondrocyte apoptosis via XXXX -mediated, redox-dependent intrinsic apoptosis pathway.

@entity1 @entity1110 @entity35 @entity4283 @entity309 @entity4210 @entity2383
UNASSIGNED: Pro-inflammatory cytokine-induced chondrocyte apoptosis is a primary cause of cartilage destruction in the progression of @entity309 ( @entity309 ). Advanced oxidation protein products (AOPPs), a novel pro-inflammatory mediator, have been confirmed to accumulate in @entity1 with @entity309 . However, the effect of AOPPs accumulation on chondrocyte apoptosis and the associated cellular mechanisms remains unclear. The present study demonstrated that the plasma formation of AOPPs was enhanced in @entity309 @entity35 compared with normal. Then, chondrocyte were treated with AOPPs-modified rat serum albumin (AOPPs-RSA) in vitro. Exposure of chondrocyte to AOPPs activated @entity1110 ( @entity1110 ) oxidase and increased expression of @entity1110 oxidase subunits, which was mediated by @entity4283 ( @entity4283 ), but not scavenger receptor @entity4210 . Moreover, AOPPs challenge triggered @entity1110 oxidase-dependent ROS generation which induced @entity2383 and endoplasmic reticulum stress resulted in activation of caspase family that eventually lead to apoptosis. Lastly, blockade of @entity4283 , instead of @entity4210 , largely attenuated these signals. Our study demonstrated first time that AOPPs induce chondrocyte apoptosis via @entity4283 -mediated and redox-dependent intrinsic apoptosis pathway in vitro. These data implicates that AOPPs may represent a novel pathogenic factor that contributes to @entity309 progression. Targeting AOPPs-triggered cellular mechanisms might emerge as a promising therapeutic option for @entity1 with @entity309 .
