%0 Journal Article
%T Micro-223 Promotes Diabetic Osteoarthritis Progression by Regulating Cartilage Degeneration and Subchondral Bone Remodeling.
%A Li Y
%A Fu T
%A Zhao Y
%A Yuan LJ
%A Wang BB
%A Guan J
%A Wang HJ
%A Li L
%A Gao YP
%J Cartilage
%V 0
%N 0
%D 2023 Nov 23
%M 37994560
%F 3.117
%R 10.1177/19476035231210631
%X <B>OBJECTIVE: </B>Our study was performed to investigate whether micro-223 promotes diabetic Osteoarthritis (OA) progression by regulating cartilage degeneration and subchondral bone remodeling.<BR><B>METHODS: </B>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.<BR><B>RESULTS: </B>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.<BR><B>CONCLUSIONS: </B>miR-223 promotes diabetic OA progression by regulating cartilage degeneration and subchondral bone remodeling both in vitro and in vivo.