Abstract：
OBJECTIVE: Our study was performed to investigate whether micro-223 promotes diabetic Osteoarthritis (OA) progression by regulating cartilage degeneration and subchondral bone remodeling.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: miR-223 promotes diabetic OA progression by regulating cartilage degeneration and subchondral bone remodeling both in vitro and in vivo.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: miR-223 promotes diabetic OA progression by regulating cartilage degeneration and subchondral bone remodeling both in vitro and in vivo.
摘要：
目的：我们的研究旨在研究micro-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。
方法：miR-223在人正常软骨中的表达，OA软骨,通过实时定量逆转录聚合酶链反应（qRT-PCR）检测有无DM的软骨下骨组织。将miR-223模拟物或抑制剂转染到软骨细胞中。通过3-（4,5）-二甲基硫代偶氮（-2）-3,5-二苯基四唑溴化物（MTT）和末端脱氧核苷酸转移酶（TdT）介导的dUTP缺口末端标记（TUNEL）测定评估细胞活力和凋亡，分别。
结果：miR-223在人糖尿病性OA软骨和软骨下骨中显著高于正常OA和健康对照。miR-223过表达加速糖尿病OA小鼠软骨退变和软骨下骨硬化,而miR-223抑制具有相反的作用。miR-223的体外上调降低了软骨细胞的增殖并增强了其凋亡。同时,miR-223的下调促进软骨细胞中糖胺聚糖（GAG）的产生。
结论：miR-223在体外和体内通过调节软骨退变和软骨下骨重建促进糖尿病性OA进展。
方法：miR-223在人正常软骨中的表达，OA软骨,通过实时定量逆转录聚合酶链反应（qRT-PCR）检测有无DM的软骨下骨组织。将miR-223模拟物或抑制剂转染到软骨细胞中。通过3-（4,5）-二甲基硫代偶氮（-2）-3,5-二苯基四唑溴化物（MTT）和末端脱氧核苷酸转移酶（TdT）介导的dUTP缺口末端标记（TUNEL）测定评估细胞活力和凋亡，分别。
结果：miR-223在人糖尿病性OA软骨和软骨下骨中显著高于正常OA和健康对照。miR-223过表达加速糖尿病OA小鼠软骨退变和软骨下骨硬化,而miR-223抑制具有相反的作用。miR-223的体外上调降低了软骨细胞的增殖并增强了其凋亡。同时,miR-223的下调促进软骨细胞中糖胺聚糖（GAG）的产生。
结论：miR-223在体外和体内通过调节软骨退变和软骨下骨重建促进糖尿病性OA进展。
