CircMYO1C silencing alleviates chondrocytes inflammation and apoptosis through m⁶A/HMGB1 axis in osteoarthritis.

IF 3.2 4区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biotechnology and applied biochemistry Pub Date : 2024-07-09 DOI:10.1002/bab.2635

Haitao Sun, Xudong Chu, Weiqing Qian, Hong Yin

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引用次数: 0

Abstract

Circular RNAs (circRNAs) are involved in osteoarthritis (OA) progression. This study aimed to investigate the role and molecular mechanisms of circMYO1C in OA. CircMYO1C was upregulated in OA- and interleukin-1β (IL-1β)-exposed chondrocytes. The results indicated that circMYO1C knockdown repressed the inflammatory factors (tumor necrosis factor alpha [TNF-α], interleukin-6 [IL-6], interleukin-8 [IL-8], etc.) and apoptosis of chondrocytes following IL-1β exposure. CircMYO1C was an N⁶-methyladenosine (m⁶A)-modified circRNA with m6A characteristics. High mobility group box 1 (HMGB1) was a target of circMYO1C. IL-1β exposure increased the stability and half-life (t_1/2) of HMGB1 mRNA, while silencing circMYO1C reduced HMGB1 mRNA stability. Taken together, circMYO1C targets the m6A/HMGB1 axis to promote chondrocyte apoptosis and inflammation. The present study demonstrates that the circMYO1C/m6A/HMGB1 axis is essential for OA progression, highlighting a novel potential therapeutic target for clinical OA.

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沉默CircMYO1C可通过m6A/HMGB1轴缓解骨关节炎中软骨细胞的炎症和凋亡。

环状 RNA（circRNA）参与骨关节炎（OA）的进展。本研究旨在探讨circMYO1C在OA中的作用和分子机制。在OA和白细胞介素-1β（IL-1β）暴露的软骨细胞中，circMYO1C被上调。结果表明，circMYO1C敲除抑制了IL-1β暴露后的炎症因子（肿瘤坏死因子α [TNF-α]、白细胞介素-6 [IL-6]、白细胞介素-8 [IL-8]等）和软骨细胞的凋亡。CircMYO1C 是一种具有 m6A 特征的 N6-甲基腺苷（m6A）修饰的 circRNA。高迁移率基团框 1（HMGB1）是 circMYO1C 的靶标。IL-1β 暴露增加了 HMGB1 mRNA 的稳定性和半衰期（t1/2），而沉默 circMYO1C 则降低了 HMGB1 mRNA 的稳定性。综上所述，circMYO1C 以 m6A/HMGB1 轴为靶标，促进软骨细胞凋亡和炎症。本研究表明，circMYO1C/m6A/HMGB1 轴对 OA 的进展至关重要，为临床治疗 OA 提供了一个新的潜在治疗靶点。

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

Biotechnology and applied biochemistry 工程技术-生化与分子生物学

CiteScore

6.00

自引率

7.10%

发文量

117

审稿时长

3 months

期刊介绍： Published since 1979, Biotechnology and Applied Biochemistry is dedicated to the rapid publication of high quality, significant research at the interface between life sciences and their technological exploitation. The Editors will consider papers for publication based on their novelty and impact as well as their contribution to the advancement of medical biotechnology and industrial biotechnology, covering cutting-edge research in synthetic biology, systems biology, metabolic engineering, bioengineering, biomaterials, biosensing, and nano-biotechnology.