PR11-364P22.2/ATF3 protein interaction mediates IL-1β-induced catabolic effects in cartilage tissue and chondrocytes.

ABSTRACT: Osteoarthritis (OA) is a degenerative joint disease which lacks effective medical treatment due to ill-defined molecular mechanisms underlying the pathology. Inflammation is a key factor that induces and aggravates OA. Therefore, the current study aims to explore roles of the dysregulated long non-coding RNAs in the pro-inflammatory cytokine IL-1β-mediated catabolic effects in cartilage tissue and chondrocytes. We identified RP11-364P22.2 as dysregulated in OA patient-derived cartilage tissues and highly responsive to IL-1β stimulus. RNA pull-down coupled with mass spectrometry demonstrated that RP11-364P22.2 physically binds to activating transcription factor 3 (ATF3) and thus increases the protein stability and facilitates its nuclear translocation. Loss- and gain-of-function assays indi

SUBMITTER: Li X 

PROVIDER: S-EPMC8256372 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature