Li Yao, Fu Ting, Zhao Yi, Yuan Long-Jie, Wang Bai-Bai, Guan Jian, Wang Hua-Jun, Li Ling, Gao Yan-Ping
Department of Orthopedics, The Third Hospital of Shijiazhuang, Shijiazhuang, China.
Department of Internal Medicine, Armed Police Corps Hospital of Hebei, Shijiazhuang, China.
Cartilage. 2023 Nov 23:19476035231210631. doi: 10.1177/19476035231210631.
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. 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 and .
本研究旨在探讨微小RNA-223（miR-223）是否通过调节软骨退变和软骨下骨重塑来促进糖尿病性骨关节炎（OA）的进展。
采用实时定量逆转录聚合酶链反应（qRT-PCR）检测miR-223在有或无糖尿病的人正常软骨、OA软骨及软骨下骨组织中的表达。将miR-223模拟物或抑制剂转染至软骨细胞。分别通过3-(4,5)-二甲基噻唑-2,5-二苯基四氮唑溴盐（MTT）法和末端脱氧核苷酸转移酶（TdT）介导的dUTP缺口末端标记（TUNEL）法评估细胞活力和凋亡情况。
与正常OA和健康对照相比，miR-223在人糖尿病性OA软骨和软骨下骨中的表达显著更高。miR-223过表达加速了糖尿病性OA小鼠的软骨退变和软骨下骨硬化，而抑制miR-223则产生相反的效果。miR-223上调降低了软骨细胞的增殖并增强了其凋亡。同时，miR-223下调促进了软骨细胞中糖胺聚糖（GAG）的产生。
miR-223通过调节软骨退变和软骨下骨重塑来促进糖尿病性OA的进展。
