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  • Title: MiR-485-3p promotes proliferation of osteoarthritis chondrocytes and inhibits apoptosis via Notch2 and the NF-κB pathway.
    Author: Zhou Y, Zhao Z, Yan L, Yang J.
    Journal: Immunopharmacol Immunotoxicol; 2021 Jun; 43(3):370-379. PubMed ID: 33961511.
    Abstract:
    CONTEXT: Osteoarthritis (OA) is one of the leading causes of disability worldwide. microRNAs (miRs) has been shown to be involved in multiple pathological processes during OA. But the possible mechanism of miR-485-3p in OA remains unclear. OBJECTIVE: This study was designed to identify the effect of miR-485-3p on OA. METHODS: miR-485-3p expression in the cartilage of OA patients and healthy controls was detected. OA cell model was established by lipopolysaccharide (LPS). miR-485-3p expression in SW1353 and CHON-001 chondrocytes treated with LPS was detected. After overexpressing miR-485-3p in chondrocytes, cell proliferation, and apoptosis were detected. Apoptosis-, extracellular matrix (ECM)-, inflammatory-, and oxidative stress-related factors were detected. The target gene of miR-485-3p was predicted by online software and verified by dual luciferase reporter gene assay. Notch2 was intervened in CHON-001 chondrocytes to detect proliferation and apoptosis. Finally, the phosphorylation of NF-κB pathway-related proteins was detected. RESULTS: miR-485-3p expression was low in OA patients and LPS-treated chondrocytes. After LPS treatment, the proliferation of SW1353 and CHON-001 chondrocytes was decreased, and apoptosis was increased. The above outcomes were reversed after overexpressing miR-485-3p. Overexpressing miR-485-3p also reduced ECM degradation, inflammation and oxidative stress in chondrocytes. miR-485-3p could target Notch2. After LPS treatment, the NF-κB pathway was activated, but miR-485-3p overexpression inhibited the pathway. Notch2 inhibition promoted proliferation and inhibited apoptosis of LPS-treated CHON-001 chondrocytes, and inhibited the NF-κB pathway. CONCLUSION: Overexpression of miR-485-3p inhibited Notch2 and the NF-κB pathway, and promoted proliferation of OA chondrocytes and inhibited apoptosis.
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