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5'tiRNA-33-CysACA-1通过准PGC-1α介导的线粒体生物生成来促进败血性心肌病

Ludong Yuan¹, Jing Li¹, Leijing Yin¹

¹Department of Pathophysiology, Sepsis Translational Medicine Key Laboratory of Hunan Province, Xiangya School of Medicine, Central South University, Changsha, Hunan 410008, China; National Medicine Functional Experimental Teaching Center, Central South University, Changsha, Hunan 410078, China.

The international journal of biochemistry & cell biology

|December 4, 2024

概括

败血性心肌病 (SCM) 涉及改变的tRNA衍生小RNAs (tsRNAs). 在SCM中升级调节的5'tiRNA-33-CysACA-1通过准PGC-1α损害了线粒体功能,促进了疾病的进展.

科学领域:

心血管生物学心血管生物学
分子生物学分子生物学
在RNA生物学,RNA生物学.

背景情况:

败血性心肌病 (SCM) 是败血症的一个严重并发症.
来自TRNA的小RNAs (tsRNAs) 与各种疾病有关,但它们在SCM中的作用在很大程度上是未知的.
微阵列分析揭示了SCM中TSRNA表达的改变.

研究的目的:

研究TSRNAs在SCM中的作用和机制.
为了确定参与SCM病原发生的特定tsRNAs.
在败血症期间探索心脏功能障碍中tsRNAs的调节网络.

主要方法:

通过结和穿孔 (CLP) 建立了鼠标败血症模型.
使用定量实时PCR (qRT-PCR) 来测量5'tiRNA-33-CysACA-1表达.
用从LPS刺激的巨细胞获得的条件介质 (CM) 对H9C2细胞进行治疗,以模拟心肌细胞损伤.
评估了细胞活力,细胞死亡,线粒体功能 (MMP,ATP,ROS) 和与线粒体质量控制相关的mRNA表达.
西方斑,mRNA稳定性测定和救援实验被用来阐明5'tiRNA-33-CysACA-1对PGC-1α的作用机制.

主要成果:

在败血性心肌损伤期间,5'tiRNA-33-CysACA-1的表达在心脏组织和H9C2细胞中显著升高.
CM治疗诱导心肌细胞损伤和线粒体功能受损.
在CM处理的细胞中,5'tiRNA-33-CysACA-1的过度表达进一步降低了氧酶增殖器激活受体马联合激活剂-1α (PGC-1α) 的表达,抑制了线粒体生物发生,并加剧了细胞死亡.
抑制5'tiRNA-33-CysACA-1可以改善这些有害影响.
mRNA稳定性测试表明,5'tiRNA-33-CysACA-1降低了PGC-1α mRNA稳定性,导致PGC-1α表达率下降.

结论:

5'tiRNA-33-CysACA-1在败血性心肌病 (SCM) 中被上调.
这种tsRNA通过准PGC-1α和降低PGC-1αmRNA稳定性来抑制线粒体生物发生.
这些行为导致线粒体功能障碍,并促进SCM的发展.

关键词:

在5'tiRNA-33-CysACA-1中.心脏肌细胞是心脏肌细胞.线粒体生物发生是线粒体生物发生.败血性心肌病 (SCM) 是一种心脏病.由TRNA衍生的小RNAs (tsRNAs) 进行检测.

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