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MiR-21通过调节HIPK3表达来减弱FAS介导的心肌细胞亡

Xinyu Wang^1,2, Tingting Zhang², Jianlong Zhai³

¹College of Postgraduate, Hebei North University, Zhangjiakou, Hebei, China.

Bioscience reports

|August 15, 2023

概括

微RNA-21 (miR-21) 通过调节HIPK3.3,保护心脏细胞免受损伤. 这一发现为急性心肌梗塞提供了潜在的新疗法.

科学领域:

心脏病学心脏病学
分子生物学分子生物学
生物化学生物化学

背景情况:

缺血-再输液损伤 (IRI) 是心脏损伤的主要原因之一.
已知microRNA-21 (miR-21) 在IRI中具有抗亡作用,但其机制尚未完全理解.
了解参与心肌细胞亡的分子途径对于开发有效的治疗方法至关重要.

研究的目的:

调查miR-21和家庭主体相互作用蛋白激酶3 (HIPK3) 在低氧/低氧化 (H/R) 诱导的心肌细胞亡中的作用.
阐明miR-21调节HIPK3并影响亡的分子机制.

主要方法:

暴露于H/R的老鼠H9C2心肌细胞系.
使用CCK-8测定,TUNEL染色和流细胞计评估的细胞活力和细胞亡.
蛋白质表达和酸化通过免疫光和西式涂抹分析.
通过qRT-PCR量化miR-21表达.
miR-21和HIPK3的相互作用通过光酶记者测定得到证实.

主要成果:

miR-21过度表达或HIPK3下调减少了H/R诱导的亡.
miR-21抑制增加了细胞灭绝.
miR-21直接准并抑制HIPK3的表达,形成一个负反循环.
下调HIPK3通过影响FADD,BAX,切割caspase-3和BCL2表达来抑制FAS介导的亡.

结论:

miR-21通过向HIPK3.3,在H/R期间减轻心肌细胞亡.
该miR-21/HIPK3通路在调节FAS介导的亡中发挥着重要作用.
这种机制对治疗急性心肌梗塞有潜在的临床影响.

关键词:

灭症 (apoptosis) 是一种死亡的过程.这是心肌细胞 (cardiomyocytes).缺氧缺氧是指缺氧的情况.这是一个微型RNA.

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