Superoxide dismutase 3 facilitates the chondrogenesis of bone marrow-derived mesenchymal stem cells

被引:10
|
作者
Shi, Yuanyuan [1 ]
Hu, Xiaoqing [1 ]
Zhang, Xin [1 ]
Cheng, Jin [1 ]
Duan, Xiaoning [1 ]
Fu, Xin [1 ]
Zhang, Jiying [1 ]
Ao, Yingfang [1 ]
机构
[1] Peking Univ, Beijing Key Lab Sports Injuries, Inst Sports Med, Hosp 3, 49 North Garden Rd, Beijing 100191, Peoples R China
基金
中国国家自然科学基金;
关键词
SOD3; Chondrogenesis; BMSCs; COLLAGEN-INDUCED ARTHRITIS; CARTILAGE REPAIR; JOINT DISEASE; RAT MODEL; AMELIORATION; EXPRESSION; M40403;
D O I
10.1016/j.bbrc.2019.01.042
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Articular cartilage defects are considered a major clinical problem because they cannot heal by themselves. To date, bone marrow-derived mesenchymal stem cells (BMSCs)-based therapy has been widely applied for cartilage repair. However, fibrocartilage was often generated after BMSC therapy; therefore, there is an urgent need to stimulate and maintain BMSCs chondrogenic differentiation. The specific role of superoxide dismutase 3 (SOD3) in chondrogenesis is unknown; therefore, the present study aimed to clarify whether SOD3 could facilitate the chondrogenic differentiation of BMSCs. We first evaluated SOD3 protein levels during chondrogenesis of BMSCs using plate cultures. We then tested whether SOD3 could facilitate chondrogenesis of BMSCs using knockdown or overexpression experiments. Increased SOD3 protein levels were observed during BMSCs chondrogenesis. SOD3 knockdown inhibited collagen type II alpha 1 chain (COL2A1), aggrecan (ACAN), and SRY-box 9 (SOX9) expression. Overexpression of SOD3 increased the levels of chondrogenesis markers (COL2A1, ACAN, and SOX9). Elevated superoxide anions were observed when SOD3 was knocked down. We concluded that SOD3 could facilitate chondrogenesis of BMSCs to improve cartilage regeneration. (C) 2019 Elsevier Inc. All rights reserved.
引用
收藏
页码:983 / 987
页数:5
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