Potential of miR-25-3p in protection of chondrocytes: emphasis on osteoarthritis.

IF 1.7 4区生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY

Folia histochemica et cytobiologica Pub Date : 2021-01-01 Epub Date: 2021-02-12 DOI:10.5603/FHC.a2021.0004

Xiao He, Lili Deng

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引用次数: 0

Abstract

Introduction: Osteoarthritis (OA) is the most prevailing musculoskeletal dysfunction triggered by lesions in synovial membranes and articular cartilage. MicroRNAs (miRNAs) have emerged as crucial regulators participated in many biological processes, such as osteoarthritis. This study was undertaken to address the role of miR-25-3p in the apoptosis of rat chondrocytes under an OA-like condition and its underlying mechanism.

Material and methods: OA cellular model was established in rat chondrocytes by TNF-a induction. Then, qRTPCR and Western blotting were utilized for evaluation of the expressions of miR-25-3p and insulin-like growth factor-binding protein 7 (IGFBP7), CCK-8 assay for inspection of chondrocyte viability, flow cytometry for assessment of cell apoptosis rate, Western blotting for the detection of cleaved caspase-3 level and dual-luciferase reporter gene assay for verification of the targeting relationship between miR-25-3p and IGFBP7.

Results: The miR-25-3p expression was decreased and IGFBP7 was elevated in TNF-a-induced rat chondrocytes. The miR-25-3p inhibited chondrocyte apoptosis and IGFBP7 promoted apoptosis as evidenced by enhanced cell viability and suppressed cell apoptosis in OA chondrocytes after miR-25-3p overexpression or IGFBP7 knockdown. The miR-25-3p facilitated chondrocyte viability and repressed cell apoptosis in OA by negatively regulating IGFBP7.

Conclusions: MiR-25-3p negatively regulates IGFBP7 to promote chondrocyte proliferation and restrain chondrocyte apoptosis. Our findings suggest that the regulation of IGFBP7 by miR-25-3p may emerge as a novel therapeutic regimen for OA.

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miR-25-3p 在保护软骨细胞方面的潜力：重点关注骨关节炎。

导言：骨关节炎（OA）是由滑膜和关节软骨损伤引发的最常见的肌肉骨骼功能障碍。微 RNA（miRNA）已成为参与许多生物过程（如骨关节炎）的关键调控因子。本研究旨在探讨 miR-25-3p 在类 OA 条件下对大鼠软骨细胞凋亡的作用及其内在机制：材料：通过 TNF-a 诱导大鼠软骨细胞建立 OA 细胞模型。方法：利用 TNF-a 诱导大鼠软骨细胞建立 OA 细胞模型，采用 qRTPCR 和 Western 印迹法检测 miR-25-3p 和胰岛素样生长因子结合蛋白 7（IGFBP7）的表达，CCK-8 检测软骨细胞活力，流式细胞术评估细胞凋亡率，Western 印迹法检测裂解的 Caspase-3 水平，双荧光素酶报告基因检测验证 miR-25-3p 和 IGFBP7 的靶向关系：结果：在TNF-a诱导的大鼠软骨细胞中，miR-25-3p表达降低，IGFBP7表达升高。过表达 miR-25-3p 或敲除 IGFBP7 后，OA 软骨细胞的细胞活力增强，细胞凋亡受到抑制，这表明 miR-25-3p 可抑制软骨细胞凋亡，而 IGFBP7 可促进细胞凋亡。miR-25-3p通过负向调节IGFBP7，促进了OA中软骨细胞的活力，抑制了细胞凋亡：MiR-25-3p通过负向调节IGFBP7促进软骨细胞增殖，抑制软骨细胞凋亡。我们的研究结果表明，miR-25-3p 对 IGFBP7 的调控可能成为治疗 OA 的一种新疗法。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Folia histochemica et cytobiologica 生物-生化与分子生物学

CiteScore

2.80

自引率

6.70%

发文量

审稿时长

6-12 weeks

期刊介绍： "Folia Histochemica et Cytobiologica" is an international, English-language journal publishing articles in the areas of histochemistry, cytochemistry and cell & tissue biology. "Folia Histochemica et Cytobiologica" was established in 1963 under the title: ‘Folia Histochemica et Cytochemica’ by the Polish Histochemical and Cytochemical Society as a journal devoted to the rapidly developing fields of histochemistry and cytochemistry. In 1984, the profile of the journal was broadened to accommodate papers dealing with cell and tissue biology, and the title was accordingly changed to "Folia Histochemica et Cytobiologica". "Folia Histochemica et Cytobiologica" is published quarterly, one volume a year, by the Polish Histochemical and Cytochemical Society.