MiR-485-3p promotes proliferation of osteoarthritis chondrocytes and inhibits apoptosis via Notch2 and the NF-κB pathway

Overexpression of miR-485-3p inhibited Notch2 and the NF-κB pathway, and promoted proliferation of OA chondrocytes and inhibited apoptosis.

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.

This study was designed to identify the effect of miR-485-3p on OA.

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.