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  • Title: miR-877-5p alleviates chondrocyte dysfunction in osteoarthritis models via repressing FOXM1.
    Author: Zhu S, Deng Y, Gao H, Huang K, Nie Z.
    Journal: J Gene Med; 2020 Nov; 22(11):e3246. PubMed ID: 32584470.
    Abstract:
    BACKGROUND: The present study aimed to investigate whether forkhead box M1 (FOXM1), as a putative target of miR-877-5p, participated in interleukin (IL)-1β-induced cartilage degeneration in experimental osteoarthritis (OA) models in vitro and in vivo. METHODS: In vitro and in vivo models of OA were established using IL-1β treated primary mouse chondrocytes and anterior cruciate ligament transection (ACLT) operation in mice. miR-877-5p mimics or agomir-miR-877-5p were used as therapeutic agents in both in vitro and in vivo models of OA. Cell viability and apoptosis were evaluated using cell counting kit-8 and terminal deoxynucleotidyl transferase dUTP nick end labeling staining, respectively. A quantitative reverse transcriptase-polymerase chain reaction and western blotting were used to measure gene and protein expression, respectively. RESULTS: FOXM1 was up-regulated in IL-1β-stimulated chondrocytes and the proximal tibia of ACLT-operated mice. Bioinformatics algorithms deduced a highly conserved sequence in the 3'-UTR of FOXM1 that could be bound with miR-877-5p. A luciferase assay indicated that miR-877-5p directly targeted the 3'-UTR of FOXM1. Overexpression of miR-877-5p could reduce protein expression of FOXM1 in chondrocytes. Concurrently, IL-1β-evoked up-regulation of FOXM1 protein expression was neutralized in chondrocytes following transfection with miR-877-5p mimics. miR-877-5p mimics or agomir-miR-887-5p could inhibit IL-1β-induced inflammation in both in vitro and in vivo models of OA. miR-877-5p might have beneficial effects on the synthesis of cartilage matrix via the promotion of SRY-box transcription factor 9 and type II collagen expression and inhibition of matrix metalloproteinase 9 expression. CONCLUSIONS: miR-877-5p can improve chondrocyte function in both in vivo and in vitro models of OA, based on post-transcriptional repression of FOXM1 as a postulated molecular mechanism.
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