MiR-30b-5p Influences Chronic Exercise Arthritic Injury by Targeting Hoxa1

Abstract

AbstractWe identified the role of miR-30b-5p in chronic exercise arthritic injury. Rats with chronic exercise arthritic injury received treatment with miR-30b-5p antagomiR. H&E and Safranin O-fast green staining were performed. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were detected. The binding relationship between homeobox A1 (Hoxa1) and miR-30b-5p was revealed. After manipulating the expressions of miR-30b-5p and/or Hoxa1 in chondrocytes, the viability, apoptosis and migration of chondrocytes were assessed. The levels of molecules were determined by qRT-PCR or Western blot. MiR-30b-5p antagomiR ameliorated articular cartilage lesion and destruction, reduced Mankin’s score and the levels of TNF-α, IL-1β, miR-30b-5p, matrix metallopeptidase 13 (MMP-13), and cleaved caspase-3, and increased relative thickness and the levels of Hoxa1, Aggrecan and type II collagen (COLII) in model rats. MiR-30b-5p up-regulation decreased Hoxa1 level, viability, migration and induced apoptosis, whereas miR-30b-5p down-regulation produced the opposite effects. MiR-30b-5p up-regulation increased the levels of MMP-13 and cleaved caspase-3, but decreased those of Aggrecan and COLII in chondrocytes. However, the action of miR-30b-5p up-regulation on chondrocytes was reversed by Hoxa1 overexpression. In conclusion, miR-30b-5p is involved in cartilage degradation in rats with chronic exercise arthritic injury and regulates chondrocyte apoptosis and migration by targeting Hoxa1.