首页> 外文期刊>Journal of cellular physiology. >Downregulation of microRNA-103a reduces microvascular endothelial cell injury in a rat model of cerebral ischemia by targeting AXIN2
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Downregulation of microRNA-103a reduces microvascular endothelial cell injury in a rat model of cerebral ischemia by targeting AXIN2

机译:Downregulation微rna - 103 a可以减少在大鼠微血管内皮细胞损伤通过针对AXIN2脑缺血模型

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Multiple microRNAs (miRNAs) have been found to be linked with cerebral ischemia. Thus, this study was employed to characterize the capabilities of miRNA-103a (miR-103a) on the brain microvascular endothelial cells (BMECs) injury in rat models of middle cerebral artery occlusion (MCAO) by regulating AXIN2. The MCAO rat model was developed by the suture method, where normal saline, miR-103a inhibitors, or its negative control were separately injected into the lateral ventricle to assess the function of miR-103a inhibitors in BMECs apoptosis, microvessel density, as well as angiogenesis. In addition, the oxygen-glucose deprivation model was induced in primarily cultured BMECs to unearth the functions of miR-103a inhibitors on cell viability and apoptosis, lactate dehydrogenase (LDH) release and tube formation ability. Furthermore, the relationship between miR-103a and AXIN2 was verified. The modeled rats of MCAO showed robustly expressed miR-103a, poorly expressed AXIN2, severe neurological deficits, accelerated apoptosis and reduced angiogenesis. miR-103a expression had a negative correlation with AXIN2 messenger RNA expression (r= -0.799; p < .05). In response to the treatment of miR-103a inhibitors, the BMECs apoptosis was suppressed and angiogenesis was restored, corresponding to upregulated Bcl-2, VEGF, and Ang-1, in addition to downregulated caspase-3 and Bax. Meanwhile, AXIN2 was verified to be the miR-103a's target gene. More important, miR-103a inhibitors led to promoted BMEC viability and tube formation and suppressed apoptosis and LDH release rate. This study highlights that miR-103a targets and negatively regulates AXIN2, whereby reducing BMEC injury in cerebral ischemia.
机译:多个小分子核糖核酸(microrna)被发现与脑缺血。是用来描述的功能microrna - 103 a (mir - 103 - a)对大脑微血管内皮细胞(BMECs)损伤大鼠模型大脑中动脉闭塞(MCAO)调节AXIN2。开发的缝合方法,正常生理盐水,mir - 103 a抑制剂或其负面控制分别注入外侧心室评估mir - 103 a的功能在BMECs凋亡抑制剂,微脉管密度,以及血管生成。oxygen-glucose剥夺模型诱导主要培养BMECs挖掘功能,mir - 103细胞抑制剂生存能力和细胞凋亡,乳酸脱氢酶(LDH)的释放和管形成能力。此外,mir - 103 a之间的关系和AXIN2验证。显示强劲表示mir - 103 a,差表示AXIN2、严重神经赤字,加速细胞凋亡和血管生成减少。mir - 103 a表达的负相关与AXIN2信使RNA表达(r = -0.799;< . 05)。抑制剂,BMECs凋亡抑制和血管再生恢复,对应调节bcl - 2、VEGF和Ang-1,除了来表达下调caspase-3和伯灵顿。AXIN2验证是mir - 103的目标基因。形成和提升BMEC可行性和管抑制细胞凋亡和LDH释放率。研究强调,mir - 103 a和目标负调节AXIN2,减少BMEC在脑缺血损伤。

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