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微小RNA-650/无翅型MMTV整合位点家族成员1在关节软骨损伤修复中的作用及机制研究

STUDY ON THE ROLE AND MECHANISM OF MICRORNA-650/WNT1 IN THE REPAIR OF ARTICULAR CARTILAGE INJURY.

作者信息

Liu Hui, Wang Yue, Wang Shuyuan, Yang Bo, Sun Di, Han Shuangyang

机构信息

Peking University Third Hospital, Qinhuangdao Hospital, Department of Nursing, Qinhuangdao, Hebei Province, China.

Peking University Third Hospital, Qinhuangdao Hospital, Department of Orthopedics, Qinhuangdao, Hebei Province, China.

出版信息

Acta Ortop Bras. 2024 Oct 7;32(4):e278218. doi: 10.1590/1413-785220243204e278218. eCollection 2024.

Abstract

OBJECTIVES

Osteoarthritis (OA) is a degenerative disease associated with chondrocyte injury. This study investigated the dysregulation of microRNA-650 (miR-650) in cartilage tissues of patients with OA. Its function and mechanism were also investigated in OA cell models.

METHODS

miR-650 levels were examined in 15 OA cartilage tissues and ten healthy cartilage tissues. SW1353 cells were used for cell function experiments and IL-1β was applied to the cells to mimic OA conditions in vitro. Cell functions such as proliferation, apoptosis, and inflammation were detected. The downstream target gene of miR-650 was identified and confirmed by bioinformatic analysis and luciferase activity assay. Rescue experiments were performed to verify the mechanism.

RESULTS

Suppressed expression of miR-650 was tested in patients with OA and cell models. Overexpression of miR-650 increased cell proliferation but suppressed apoptosis and inflammation of SW1353. As the target gene of miR-650, WNT1 overexpression counteracted the role of miR-650 in the function of SW1353.

CONCLUSION

miR-650 can protect against articular cartilage injury in OA by targeting WNT1.

摘要

目的

骨关节炎(OA)是一种与软骨细胞损伤相关的退行性疾病。本研究调查了OA患者软骨组织中微小RNA-650(miR-650)的失调情况。还在OA细胞模型中研究了其功能和机制。

方法

检测了15例OA软骨组织和10例健康软骨组织中的miR-650水平。使用SW1353细胞进行细胞功能实验,并向细胞中施加白细胞介素-1β(IL-1β)以模拟体外OA条件。检测细胞增殖、凋亡和炎症等细胞功能。通过生物信息学分析和荧光素酶活性测定鉴定并确认了miR-650的下游靶基因。进行了拯救实验以验证机制。

结果

在OA患者和细胞模型中检测到miR-650表达受到抑制。miR-650的过表达增加了细胞增殖,但抑制了SW1353的凋亡和炎症。作为miR-650的靶基因,WNT1的过表达抵消了miR-650在SW1353功能中的作用。

结论

miR-650可通过靶向WNT1来保护OA中的关节软骨损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d4/11460656/f4c8cfbdfadb/1809-4406-aob-32-04-e278218-f1.jpg

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