miR-129-3p alleviates chondrocyte apoptosis in knee joint fracture-induced osteoarthritis through CPEB1

Background Osteoarthritis (OA), a refractory disease, is one of the leading contributors for disability worldwide. Since chondrocyte is the only resident cell in cartilage, this study aims to explore the roles of miR-129-3p and CPEB1 in chondrocyte apoptosis in knee joint fracture-induced OA. Method...

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Published in:Journal of orthopaedic surgery and research 2020-11, Vol.15 (1), p.1-552, Article 552
Main Authors: Chen, Ruixiong, Ye, Baoqing, Xie, Han, Huang, Yuliang, Wu, Zhehui, Wu, Hongbo, Wang, Xiaofeng, Miao, Haixiong, Liang, Weiguo
Format: Article
Language:English
Subjects:
Analysis
Apoptosis
Arthritis
Cancer
Cartilage
Cartilage diseases
Caspase-3
Cell viability
Chondrocytes
Collagen
Collagen (type II)
Fractures
Joint surgery
Males
MicroRNAs
Orthopedics
Osteoarthritis
Toluidine
Tumor necrosis factor-α
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Summary:Background Osteoarthritis (OA), a refractory disease, is one of the leading contributors for disability worldwide. Since chondrocyte is the only resident cell in cartilage, this study aims to explore the roles of miR-129-3p and CPEB1 in chondrocyte apoptosis in knee joint fracture-induced OA. Methods Cartilage was collected from 20 OA patients who underwent total knee replacement (OA group) and 20 patients with knee contusion (normal group). Then, miR-129-3p and CPEB1 levels in the cartilage were quantified by qRT-PCR. Primary rat chondrocytes in the knee were isolated and identified by toluidine blue staining and immunofluorescent staining of type II collagen. OA cellular models were induced by TNF-[alpha] treatment, in which miR-129-3p and CPEB1 expressions were assessed. Subsequently, cell viability, apoptosis, and the expression levels of apoptotic protein and caspase-3 were measured. Dual luciferase reporter assay identified the interaction between miR-129-3p and CPEB1. Results Patients in the OA group had decreased miR-129-3p expression and increased CPEB1 expression than those in the normal group. TNF-[alpha] treatment successfully induced the OA cellular model. Downregulated miR-129-3p and upregulated CPEB1 expressions were found in OA-treated chondrocytes. miR-129-3p overexpression or CPEB1 knockdown improved chondrocyte viability and attenuated apoptosis, and vice versa. miR-129-3p negatively regulated CPEB1, thus ameliorating apoptosis and enhancing cell viability. Conclusion miR-129-3p negatively targeted CPEB1 to facilitate chondrocyte viability and hamper apoptosis. Keywords: miR-129-3p, CPEB1, Knee joint fracture, Osteoarthritis, Cell viability, Chondrocyte apoptosis
ISSN:1749-799X
1749-799X
DOI:10.1186/s13018-020-02070-1