MicroRNA-26a 通过靶向 PTEN 调节脑缺血损伤。
MicroRNA-26a regulates cerebral ischemia injury through targeting PTEN.
机构信息
Department of Neurology, Yantai City Yantai Mountain Hospital, Yantai, China.
出版信息
Eur Rev Med Pharmacol Sci. 2019 Aug;23(16):7033-7041. doi: 10.26355/eurrev_201908_18745.
OBJECTIVE
MicroRNA-26a (miR-26a) exhibits diverse functions in different human disease. However, further research is needed to investigate the potential role of miR-26a in cerebral ischemia injury.
MATERIALS AND METHODS
The expressions of miR-26a and PTEN (phosphatase and tensin homolog) were detected via Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) assay. The protein expression of Bcl-2 and Bax was detected by Western blot assay. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was used to observe the cell viability of SH-SY5Y cells. The relationship between miR-26a and PTEN was confirmed by Dual-Luciferase assay and human SH-SY5Y cells were treated with oxygen-glucose deprivation (OGD)/reperfusion to mimic I/R injury.
RESULTS
The expression of miR-26a was increased in the OGDR model. Moreover, upregulation of miR-26a promoted cell viability and inhibited OGDR-induced apoptosis. PTEN was confirmed as a direct target gene for miR-26a. Under OGDR conditions, the expression of PTEN was significantly decreased. Moreover, overexpression of PTEN inhibited cell viability, promoted cell apoptosis and deepened the effect of the OGDR model.
CONCLUSIONS
MiR-26a promoted the viability of SH-SY5Y cells and suppressed apoptosis under OGDR conditions by targeting PTEN.
目的
MicroRNA-26a（miR-26a）在不同的人类疾病中表现出多种功能。然而，需要进一步的研究来探讨 miR-26a 在脑缺血损伤中的潜在作用。
材料与方法
通过实时定量聚合酶链反应（RT-qPCR）检测 miR-26a 和 PTEN（磷酸酶和张力蛋白同源物）的表达。通过 Western blot 检测 Bcl-2 和 Bax 的蛋白表达。MTT（3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐）检测观察 SH-SY5Y 细胞的细胞活力。通过双荧光素酶报告基因实验证实 miR-26a 与 PTEN 之间的关系，并用人 SH-SY5Y 细胞进行氧葡萄糖剥夺（OGD）/再灌注以模拟 I/R 损伤。
结果
在 OGDR 模型中，miR-26a 的表达增加。此外，miR-26a 的上调促进了细胞活力并抑制了 OGDR 诱导的细胞凋亡。PTEN 被证实是 miR-26a 的直接靶基因。在 OGDR 条件下，PTEN 的表达明显降低。此外，PTEN 的过表达抑制了细胞活力，促进了细胞凋亡，并加深了 OGDR 模型的作用。
结论
miR-26a 通过靶向 PTEN 促进 SH-SY5Y 细胞在 OGDR 条件下的活力并抑制细胞凋亡。
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