Gene ( IF 3.5 ) Pub Date : 2020-09-16 , DOI: 10.1016/j.gene.2020.145148 Wu Zhang 1 , Yuqin Wu 1 , Hong Chen 1 , Dan Yu 2 , Jinfeng Zhao 3 , Jing Chen 1
Ischemic stroke is a common clinical cardiovascular disease and often accompanied by central nervous system injury. It often causes paralysis or loss of motor function after central nervous system injury and significantly reduces the patient’s quality of life. At present, there is no effective treatment strategy for nerve damage caused by ischemic stroke. Therefore, it is urgently need to explore effective treatment targets. The protein expression of SOX5, VEGF and apoptosis related proteins were measured by western blot. The mRNA expression of SOX5 and VEGF were detected by RT-qPCR. The concentration of S100B and GFAP which are related to nerve damage were detected using ELISA assay. The transcriptional regulation of SOX5 on VEGF was detected using ChIP-PCR and dual luciferase reporter gene assays. The cell apoptosis was measured by TUNEL assay and cell viability was detected by CCK-8 assay. In our study, we found that the expression of SOX5 was significantly reduced when LPS induced apoptosis in PC-12 cells. Overexpression of SOX5 repaired LPS-induced apoptosis. SOX5 promotes VEGF expression as a transcription factor to activate the PI3K/AKT pathway. VEGF also repairs nerve injury and brain tissue injury caused by ischemic stroke. In conclusion, SOX5 transcription regulates the expression of VEGF to activate the PI3K/AKT pathway, which repaired nerve damage caused by ischemic stroke. Therefore, SOX5 could be a new target to regulate VEGF which can repair nerve injury induced by ischemic stroke.
中文翻译:
SOX5通过调节VEGF / PI3K / AKT途径对缺血性中风的神经保护作用。
缺血性中风是一种常见的临床心血管疾病,通常伴有中枢神经系统损伤。在中枢神经系统受伤后,它通常会导致瘫痪或运动功能丧失,并显着降低患者的生活质量。目前,尚无针对缺血性中风引起的神经损伤的有效治疗策略。因此,迫切需要探索有效的治疗目标。Western blot检测SOX5,VEGF和凋亡相关蛋白的表达。RT-qPCR检测SOX5和VEGF的mRNA表达。用ELISA法检测与神经损伤有关的S100B和GFAP的浓度。使用ChIP-PCR和双荧光素酶报告基因检测了SOX5对VEGF的转录调控。用TUNEL法检测细胞凋亡,用CCK-8法检测细胞活力。在我们的研究中,我们发现当LPS诱导PC-12细胞凋亡时,SOX5的表达显着降低。SOX5的过表达修复LPS诱导的细胞凋亡。SOX5促进VEGF表达作为激活PI3K / AKT途径的转录因子。VEGF还修复由缺血性中风引起的神经损伤和脑组织损伤。总之,SOX5转录调节VEGF的表达以激活PI3K / AKT途径,从而修复缺血性中风引起的神经损伤。因此,SOX5可能成为调节VEGF的新靶点,它可以修复缺血性中风引起的神经损伤。我们发现,LPS诱导PC-12细胞凋亡时,SOX5的表达显着降低。SOX5的过表达修复LPS诱导的细胞凋亡。SOX5促进VEGF表达作为激活PI3K / AKT途径的转录因子。VEGF还修复由缺血性中风引起的神经损伤和脑组织损伤。总之,SOX5转录调节VEGF的表达以激活PI3K / AKT途径,从而修复缺血性中风引起的神经损伤。因此,SOX5可能成为调节VEGF的新靶点,它可以修复缺血性中风引起的神经损伤。我们发现,LPS诱导PC-12细胞凋亡时,SOX5的表达显着降低。SOX5的过表达修复LPS诱导的细胞凋亡。SOX5促进VEGF表达作为激活PI3K / AKT途径的转录因子。VEGF还修复由缺血性中风引起的神经损伤和脑组织损伤。总之,SOX5转录调节VEGF的表达以激活PI3K / AKT途径,从而修复缺血性中风引起的神经损伤。因此,SOX5可能成为调节VEGF的新靶点,它可以修复缺血性中风引起的神经损伤。SOX5转录调节VEGF的表达以激活PI3K / AKT途径,从而修复缺血性中风引起的神经损伤。因此,SOX5可能成为调节VEGF的新靶标,可以修复缺血性中风所致的神经损伤。SOX5转录调节VEGF的表达以激活PI3K / AKT途径,从而修复缺血性中风引起的神经损伤。因此,SOX5可能成为调节VEGF的新靶点,它可以修复缺血性中风引起的神经损伤。