循环RNA SEC24A 通过 miR-107-5p/CASP3 轴促进骨关节炎
Tuerxunjiang Dadihanc1,2, Yong Zhang3, Guo-Qing Li2
1State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, Xinjiang Province, PR China.
Regenerative therapy
|June 3, 2024
概括
循环RNA SEC24A (circSEC24A) 通过海绵化miR-107-5p促进骨关节炎 (OA),导致CASP3表达增加和矩阵降解. 沉默circSEC24A可以缓解OA的进展.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 骨关节炎 (OA) 是一种常见的慢性关节疾病.
- 循环RNA SEC24A (circSEC24A) 的表达在OA软骨细胞中升高.
- circSEC24A在OA发病过程中的确切作用尚不清楚.
研究的目的:
- 为了阐明circSEC24A在骨关节炎中的功能.
- 研究circSEC24A在OA中的作用背后的分子机制.
- 探索circSEC24A作为OA的潜在治疗点.
主要方法:
- 生物信息分析预测了一个circRNA-miRNA-mRNA网络.
- 在体外OA慢性细胞模型被IL-1β诱导.
- 使用qRT-PCR和西布洛特测量了circSEC24A,miR-107-5p和CASP3的表达水平.
- 评估了细胞活力,细胞亡和细胞外基质 (ECM) 降解.
- 路西费拉斯报告员和RIP测定证实了分子相互作用.
- 使用前十字带切割 (ACLT) 鼠标模型来评估体内效应.
主要成果:
- 在CircSEC24A和CASP3水平上调,而miR-107-5p在OA软骨和软骨细胞下调.
- CircSEC24A作为miR-107-5p的分子海绵起作用.
- 击败circSEC24A抑制了冠状细胞亡,ECM降解和炎症.
- CASP3被确定为miR-107-5p的直接目标.
- 通过准CASP3.3,米R-107-5p模仿者可以防止OA的进展.
- 沉默circSEC24A在ACLT大鼠模型中改善了OA的进展.
结论:
- CircSEC24A促进了骨关节炎的进展.
- 该机制涉及circSEC24A海绵式miR-107-5p,导致CASP3表达的增加.
- 针对circSEC24A/miR-107-5p/CASP3轴可能为OA提供治疗策略.
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