Long non-coding ribonucleic acid AFAP1-AS1 promotes chondrocyte proliferation via the miR-512-3p/matrix metallopeptidase 13 (MMP-13) axis

Long-chain non-coding RNAs are reported to be involved in cartilage damage. However, less research on the role of actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) in osteoarthritis. To investigate AFAP1-AS1 function in osteoarthritis development, AFAP1-AS1 and miR-512-3p expression levels in osteoarthritis cartilage and cells were evaluated using RT-qPCR. The downstream target genes of AFAP1-AS1 and miR-512-3p were predicted and validated using luciferase reporter assays. Moreover, a knee osteoarthritis model was established by injecting monoiodoacetate into the knee joints of mice. The effects of AFAP1-AS1 and miR-512-3p on osteoarthritis chondrocyte proliferation and MMP-13, collagen II, and collagen IV expressions were detected in vivo using CCK-8 assay and Western blotting and RT-qPCR, respectively. AFAP1-AS1 expression was upregulated in osteoarthritis cartilage and cells. MiR-512-3p expression was downregulated in osteoarthritis cartilage. AFAP1-AS1 overexpression inhibited miR-512-3p expression in chondrocytes. Furthermore, AFAP1-AS1 over-expression promoted chondrocyte proliferation, and miR-512-3p mimic inhibited chondrocyte proliferation in vivo. AFAP1-AS1 overexpression reduced type II and type IV collagen expression, while miR-512-3p overexpression promoted type II and type IV collagen in vivo. AFAP1-AS1 overexpression enhanced MMP-13 expression in vivo. AFAP1-AS1 overexpression regulated chondrocyte proliferation by inhibiting miR-512-3p expression in vivo. AFAP1-AS1 could be a potential target to treat osteoarthritis by inhibiting miR-512-3p and subsequently inducing chondrocyte proliferation and regulating matrix synthesis.

Automated summary

Research has shown that overexpression of AFAP1-AS1 promotes chondrocyte proliferation, inhibits miR-512-3p expression, and regulates matrix synthesis in osteoarthritis.