Micro-223 Promotes Diabetic Osteoarthritis Progression by Regulating Cartilage Degeneration and Subchondral Bone Remodeling.

Abstract

Our study was performed to investigate whether micro-223 promotes diabetic Osteoarthritis (OA) progression by regulating cartilage degeneration and subchondral bone remodeling. The expression of miR-223 in human normal cartilage, OA cartilage, and subchondral bone tissue with or without DM was detected by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). miR-223 mimic or inhibitor was transfected into chondrocytes. Cell viability and apoptosis were assessed by 3-(4,5)-dimethylthiahiazo(-2)-3,5-diphenyltetrazolium bromide (MTT) and Terminal Deoxynucleotidyl Transferase(TdT)-mediated dUTP nick end labeling (TUNEL) assay, respectively. miR-223 was significantly higher in human diabetic OA cartilage and subchondral bone compared with normal OA and healthy control. Overexpression of miR-223 accelerated cartilage degeneration and subchondral bone sclerosis in diabetic OA mice, whereas miR-223 inhibition had the opposite effect. In vitro upregulation of miR-223 decreased proliferation and enhanced apoptosis of chondrocytes. Meanwhile, downregulation of miR-223 promoted glycosaminoglycan (GAG) production in chondrocytes. miR-223 promotes diabetic OA progression by regulating cartilage degeneration and subchondral bone remodeling both in vitro and in vivo.