MiR-124 regulates apoptosis in hypoxia-induced human brain microvessel endothelial cells through targeting Bim

被引:0
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作者
Jie Pu
Yuan Long
Jian Zhou
Yanqiang Zhan
Xiaoyong Qin
机构
[1] Renmin Hospital of Wuhan University & Hubei General Hospital,Department of Neurosurgery
[2] Wuhan Children’s Hospital,Department of Cardiovascular Medicine
[3] Tongji Medical College,Department of Stomatology
[4] Huazhong University of Science and Technology,Department of Neurosurgery
[5] the 253rd Hospital of Chinese People’s Liberation Army,undefined
[6] the 253rd Hospital of Chinese People’s Liberation Army,undefined
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关键词
Apoptosis; Bim; MiR-124; Stroke;
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暂无
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学科分类号
摘要
Human brain microvessel endothelial cells (HBMECs) are crucial for brain vascular repair and maintenance. The high-expressed expressions of microRNA-124 (miR-124) in brain have been investigated and revealed in many researches. In this work, we aimed to investigate the role of miR-124 in apoptosis of HBMECs and the underlying mechanism. Here, we found the low-expressed miR-124 in hypoxia-induced HBMECs using qRT-PCR analysis. MiR-124 targeting 3′-untranslated region (3′-UTR) of Bim mRNA was predicted by Targetscan database. Importantly, the decreased miR-124 expression and increased Bim expression, an opposite trend, were obtained in hypoxia-induced HBMECs. The further confirmation of the correlation between miR-124 and Bim was conducted by miR-124 overexpression and dual luciferase reporter assays. The inhibitory role of miR-124 in Bim expression was evidenced by results obtained from miR-124 overexpression analysis. Luciferase reporter assay further proved that miR-124 directly targeted the two conserved seed sites in the Bim 3′-UTR. The inhibited apoptosis of HBMECs was observed under both miR-124 overexpression and Bim knockdown condition in flow cytometry analysis. Collectively, these findings outline that miR-124 regulates apoptosis in hypoxia-induced HBMECs through targeting Bim, providing a better understanding of the role of miR-124 in apoptosis of HBMECs.
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页码:689 / 696
页数:7
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