Aging · 2019 · 29 citations · 41 references
Life SciencesCell BiologyImmunologyCell SignalingInflammationSignal TransductionCartilage BreakdownCartilage DegenerationInflammatory SignalingJoint DiseaseJoint PathologyOsteoarthritisArticular Cartilage LossC-jun N-terminal Kinase SignalingCartilage Breakdown PathophysiologyCartilage Degradation MechanismsCartilage DestructionMatrix MetalloproteinasesMyeloid Differentiation Primary Response 88 SignalingReceptor Serine/threonine Kinase Signaling
. RIPK1 was required for myeloid differentiation primary response 88 (MyD88)- and TIR-domain-containing adapter-inducing interferon b (TRIF)-mediated production of matrix metalloproteinases (MMPs) in OA. Moreover, overexpression of RIPK1 promoted the expression of tumor necrosis factor receptor-associated factor 2 (TRAF2), which blocked the expression and phosphorylation of RIPK1. Upregulation of TRAF2 decreased the expression of TRIF, MyD88, and MMPs in chondrocytes. Furthermore, knockdown of RIPK1 blocked activation of the nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK) signaling pathways. In summary, knockdown of RIPK1 alleviated OA in a manner mediated by the TRIF/MyD88-RIPK1-TRAF2 negative feedback loop and activation of the NF-κB and JNK signaling pathways.
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