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长非编码RNAGlis2通过海绵化miR-328-5pp调节了糖尿病病中的细胞线粒体功能障碍和亡

Ting Wang¹, Yanxia Chen¹, Zhihong Liu¹

¹Department of Endocrinology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, P.R. China.

Journal of cellular and molecular medicine

|March 20, 2024

概括

长非编码RNA Glis2 (lncRNA Glis2) 通过减少 podocyte 亡来防止糖尿病病 (DN). 它作为miR-328-5p的竞争RNA,改善线粒体功能并减轻DN进展.

科学领域:

分子生物学分子生物学
腎臟病學 (nephrology) 是一種醫學專業.
遗传学是一个遗传学.

背景情况:

足细胞亡是糖尿病病 (DN) 发病的一个关键因素.
长非编码RNAs (lncRNAs) 越来越多地被认为是它们在细胞亡中的作用,包括 podocytes.

研究的目的:

研究 lncRNA Glis2 在调节 DN 中 podocyte 亡中的作用.
阐明DN中lncRNA Glis2的潜在分子机制.

主要方法:

流细胞计用于检测亡速率.
对于线粒体膜潜力 (ΔΨM) 评估的 JC-1 染色.
线粒体形态的深红色染色.
定期酸-Schiff (PAS) 染色和传输电子显微镜用于脏组织分析.
双 luciferase 记者测定以确认 lncRNA Glis2 和 miR-328-5p 之间的直接相互作用.

主要成果:

在高葡萄糖培养的葡萄细胞和糖尿病小鼠脏中,lncRNA Glis2显著下调.
过度表达lncRNA Glis2缓解了细胞的线粒体功能障碍和亡.
lncRNA Glis2与miR-328-5p直接相互作用.
在糖尿病小鼠模型中,lncRNA Glis2的过度表达减少了 podocyte 亡.

结论:

lncRNA Glis2 作为对 miR-328-5p.p. 的竞争性内源RNA (ceRNA) 作用.
lncRNA Glis2调节DN中的Sirt1介导的线粒体功能障碍和细胞亡.
lncRNA Glis2证明了糖尿病病的治疗潜力.

关键词:

竞争的内源性RNA (ceRNA) 是一种竞争的内源性RNA.糖尿病病 (DN) 是一种疾病.长非编码RNAs (lncRNAs) 是一种长非编码RNA.线粒体功能障碍线粒体功能障碍波多细胞亡 (podocyte apoptosis) 是一种细胞亡的过程.

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