骨关节炎
软骨
软骨细胞
发病机制
信使核糖核酸
RNA干扰
小RNA
化学
细胞生物学
癌症研究
医学
核糖核酸
生物
基因
病理
解剖
生物化学
替代医学
作者
Hongyu Chen,Zhuli Qu,Tingting Shi,Huaqiang Zhao,Shengdong Huang,Chuan Ma
出处
期刊:Oral Diseases
[Wiley]
日期:2024-01-02
卷期号:30 (7): 4440-4453
被引量:2
摘要
Abstract Objectives The pathogenesis of temporomandibular joint osteoarthritis (TMJOA) remains not fully understood. Our previous studies demonstrated that miR‐21‐5p may participate in the TMJOA development and the interaction between circRNA‐ACAP2 (CircACAP2) and miR‐21‐5p. Our present study aimed to explore the biological functions and regulatory mechanisms of CircACAP2 in TMJOA. Materials and Methods The differential expression pattern of CircACAP2 in OA and normal tissues or cells was detected. CircACAP2 biological functions experiments were performed in chondrocytes by overexpression and interference techniques. The interaction of CircACAP2 with miR‐21‐5p and downstream target mRNA, polymorphic adenoma gene 1 (PLAG1), was predicted by bioinformatic databases and then demonstrated by dual‐luciferase reporter assay. The biological role of CircACAP2 in TMJOA was investigated and validated in a mouse model. Results The expression level of CircACAP2 was markedly reduced in OA cartilage and directly related to chondrocyte proliferation and apoptosis as well as ECM metabolism in the cartilage. CircACAP2 functioned in chondrocytes via targeting miR‐21‐5p and PLAG1. Overexpressing of CircACAP2 alleviated TMJOA in mouse models. Conclusions The present study unveiled that CircACAP2/miR‐21‐5p/PLAG1 axis may play an important regulatory role in TMJOA progression, which may highlight a potentially effective intervention and therapeutic strategy for the treatment of TMJOA.
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