循环RNACircDHRS3通过调解MECP2表达来加剧IL-1β诱导的ECM退化,亡和炎症反应
Xiao Ouyang1, Yunzhi Ding2, Li Yu2
1Department of Orthopedic Surgery, Xuzhou Third People's Hospital, Affiliated Xuzhou Hospital of Jiangsu University, No.131, Huancheng Road, Gulou, Xuzhou, 221005, Jiangsu, China. ou1yangxiao@163.com.
Inflammation
|June 20, 2023
概括
循环RNAcircDHRS3和MECP2是上调的,而miR-193a-3p在骨关节炎中是下调的. 循环DHRS3通过海绵化miR-193a-3p加剧胆固醇细胞损伤,增加MECP2的表达.
科学领域:
- 分子生物学分子生物学
- 生物化学 生物化学
- 遗传学 遗传学 是一个
背景情况:
- 骨关节炎 (OA) 的发病包括基因表达失调.
- 循环RNA hsa_circ_0010024 (circDHRS3),微RNA (miR)-193a-3p和甲基CpG结合蛋白2 (MECP2) 在OA软骨中显示出改变的表达.
- 在OA中,circDHRS3,miR-193a-3p和MECP2之间的精确调节网络仍然不清楚.
研究的目的:
- 为了阐明circDHRS3,miR-193a-3p和MECP2在骨关节炎中的调节机制.
- 为了研究circDHRS3/miR-193a-3p/MECP2轴在状细胞损伤中的作用.
主要方法:
- 定量实时PCR (qRT-PCR) 用于基因表达分析.
- 西方涂抹用于蛋白质水平评估.
- 细胞检测包括扩散 (EdU,细胞计数),亡 (流细胞计量) 和炎症性细胞因子检测 (ELISA).
- 双露西法酶记者测定以验证分子相互作用.
主要成果:
- 在OA软骨中,CircDHRS3和MECP2显著上调,而miR-193a-3p在OA软骨中显著下调.
- 循环DHRS3沉默减弱了IL-1β诱导的慢性细胞亡,细胞外矩阵降解和炎症.
- CircDHRS3作为miR-193a-3p的分子海绵,从而调节MECP2的表达.
- miR-193a-3p的抑制抵消了circDHRS3沉默的保护作用,MECP2的过度表达逆转了miR-193a-3p模仿对状细胞损伤的抑制作用.
结论:
- CircDHRS3通过菌miR-193a-3p和上调MECP2.2,促进骨关节炎的进展.
- 环DHRS3 / miR-193a-3p / MECP2轴代表了骨关节炎治疗的潜在治疗标.
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