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通过靶向Bhlhe40上调miR-494-3p会加剧脑缺血损伤。

MiR-494-3p Upregulation Exacerbates Cerebral Ischemia Injury by Targeting Bhlhe40.

作者信息

Sun Lingjiang, Ji Dandan, Zhi Feng, Fang Yu, Zhu Zigang, Ni Tong, Zhu Qin, Bao Jie

机构信息

Department of Critical Care Medicine, Wuxi Second People's Hospital, Wuxi, Jiangsu, China.

Department of Stomatology, Taixing Third People's Hospital, Taizhou, Jiangsu, China.

出版信息

Yonsei Med J. 2022 Apr;63(4):389-398. doi: 10.3349/ymj.2022.63.4.389.

DOI:10.3349/ymj.2022.63.4.389
PMID:35352891
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8965425/
Abstract

PURPOSE

Cerebral ischemia is related to insufficient blood supply and is characterized by abnormal reactive oxygen species (ROS) production and cell apoptosis. Previous studies have revealed a key role for basic helix-loop-helix family member e40 (Bhlhe40) in oxidative stress and cell apoptosis. This study aimed to investigate the roles of miR-494-3p in cerebral ischemia/reperfusion (I/R) injury.

MATERIALS AND METHODS

A mouse middle cerebral artery occlusion (MCAO/R) model was established to mimic cerebral ischemia in vivo. Brain infarct area was assessed using triphenyl tetrazolium chloride staining. Oxygen-glucose deprivation/reoxygenation (OGD/R) operation was adopted to mimic neuronal injury in vitro. Cell apoptosis was analyzed by flow cytometry. The relationship between miR-494-3p and Bhlhe40 was validated by luciferase reporter and RNA immunoprecipitation assays.

RESULTS

Bhlhe40 expression was downregulated both in MCAO/R animal models and OGD/R-induced SH-SY5Y cells. Bhlhe40 overexpression inhibited cell apoptosis and reduced ROS production in SH-SY5Y cells after OGD/R treatment. MiR-494-3p was verified to bind to Bhlhe40 and negatively regulate Bhlhe40 expression. Additionally, cell apoptosis and ROS production in OGD/R-treated SH-SY5Y cells were accelerated by miR-494-3p overexpression. Rescue experiments suggested that Bhlhe40 could reverse the effects of miR-494-3p overexpression on ROS production and cell apoptosis.

CONCLUSION

MiR-494-3p exacerbates brain injury and neuronal injury by regulating Bhlhe40 after I/R.

摘要

目的

脑缺血与血液供应不足有关，其特征是活性氧（ROS）产生异常和细胞凋亡。先前的研究已经揭示了碱性螺旋-环-螺旋家族成员e40（Bhlhe40）在氧化应激和细胞凋亡中的关键作用。本研究旨在探讨miR-494-3p在脑缺血/再灌注（I/R）损伤中的作用。

材料与方法

建立小鼠大脑中动脉闭塞（MCAO/R）模型以模拟体内脑缺血。使用氯化三苯基四氮唑染色评估脑梗死面积。采用氧糖剥夺/复氧（OGD/R）操作模拟体外神经元损伤。通过流式细胞术分析细胞凋亡。通过荧光素酶报告基因和RNA免疫沉淀试验验证miR-494-3p与Bhlhe40之间的关系。

结果

在MCAO/R动物模型和OGD/R诱导的SH-SY5Y细胞中，Bhlhe40表达均下调。Bhlhe40过表达抑制了OGD/R处理后SH-SY5Y细胞的凋亡并减少了ROS的产生。验证miR-494-3p与Bhlhe40结合并负向调节Bhlhe40表达。此外，miR-494-3p过表达加速了OGD/R处理的SH-SY5Y细胞中的细胞凋亡和ROS产生。挽救实验表明，Bhlhe40可以逆转miR-494-3p过表达对ROS产生和细胞凋亡的影响。

结论

miR-494-3p在I/R后通过调节Bhlhe40加重脑损伤和神经元损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b6/8965425/4eefd757e96f/ymj-63-389-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b6/8965425/02f818520fe4/ymj-63-389-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b6/8965425/65a1508257ad/ymj-63-389-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b6/8965425/4eefd757e96f/ymj-63-389-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b6/8965425/02f818520fe4/ymj-63-389-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b6/8965425/65a1508257ad/ymj-63-389-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b6/8965425/6e4597b17a6f/ymj-63-389-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b6/8965425/2a5e9124d1a2/ymj-63-389-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c2b6/8965425/4eefd757e96f/ymj-63-389-g005.jpg

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