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微小RNA-30b在骨关节炎中的表达上调及其在软骨细胞ERG调控中的作用

Elevated expression of microRNA-30b in osteoarthritis and its role in ERG regulation of chondrocyte.

作者信息

Li Lisong, Yang Cao, Liu Xianzhe, Yang Shuhua, Ye Shunan, Jia Jie, Liu Wei, Zhang Yukun

机构信息

Department of Orthopedics, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.

Department of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

出版信息

Biomed Pharmacother. 2015 Dec;76:94-9. doi: 10.1016/j.biopha.2015.10.014. Epub 2015 Nov 12.

Abstract

ERG (ETS-related gene) belongs to the ETS family of transcription factors, and has been recently reported to contribute to homeostatic balance in skeleton cell plasticity. MicroRNA-30 (miR-30) family is also demonstrated to play a role in controlling chondrocyte differentiation. The current study investigated the miR-30b and ERG expression in articular cartilage of osteoarthritis (OA) patients. A total of 20 subjects, with 10 OA patients and 10 healthy participants, were included in this study. Human chondrosarcoma cell line SW1353 was used to explore the relationship of miR-30b and ERG in vitro. In OA patients, a significant increase of miR-30b and a decrease of ERG were observed in articular cartilage compared with Normal ones. MiR-30b mimic down-regulated the ERG mRNA and protein expression levels, while miR-30b inhibitor up-regulated ERG expression. In addition, miR-30b mimic also decreased the mRNA expression of COL2a and aggrecan, while miR-30b inhibitor had the opposite effect. Luciferase reporter assay confirmed that miR-30b targeted ERG. In conclusion, miR-30b was involved in the process of OA, and it probably functioned through its target gene ERG.

摘要

ERG(ETS相关基因)属于ETS转录因子家族,最近有报道称其有助于维持骨骼细胞可塑性的稳态平衡。MicroRNA - 30(miR - 30)家族也被证明在控制软骨细胞分化中发挥作用。本研究调查了骨关节炎(OA)患者关节软骨中miR - 30b和ERG的表达情况。本研究共纳入20名受试者,其中10名OA患者和10名健康参与者。使用人软骨肉瘤细胞系SW1353在体外探索miR - 30b与ERG的关系。与正常受试者相比,OA患者关节软骨中miR - 30b显著增加,ERG减少。miR - 30b模拟物下调ERG mRNA和蛋白表达水平,而miR - 30b抑制剂上调ERG表达。此外,miR - 30b模拟物还降低了COL2a和聚集蛋白聚糖的mRNA表达,而miR - 30b抑制剂则有相反的作用。荧光素酶报告基因检测证实miR - 30b靶向ERG。总之,miR - 30b参与了OA的发病过程,并且可能通过其靶基因ERG发挥作用。

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