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作 者:郭涛 石亚伟 GUO Tao;SHI Yawei(Institute of Biotechnology,Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education,Shanxi University,Taiyuan 030006,China)
机构地区:[1]山西大学生物技术研究所,化学生物学与分子工程教育部重点实验室,山西太原030006
出 处:《山西大学学报(自然科学版)》2023年第2期457-466,共10页Journal of Shanxi University(Natural Science Edition)
基 金:国家自然科学基金(31170748)。
摘 要:施旺细胞参与髓鞘的形成与神经损伤后再生,涉及细胞的增殖和迁移能力。Ezrin蛋白对施旺细胞增殖和迁移的调控机制尚不明确。本文在RSC96细胞中对Ezrin基因干扰和过表达,结合qRT-PCR技术、MMT法、western印迹法和细胞划痕实验,检测Ezrin表达量的变化对RSC96细胞增殖和迁移能力的影响。结果显示Ezrin表达下调能够显著抑制RSC96细胞的增殖和迁移能力,过表达Ezrin则不影响RSC96细胞增殖能力但明显提高其迁移能力。此外,利用Y27632抑制剂降低Ezrin的Thr567磷酸化水平,同样不影响RSC96细胞增殖,但显著抑制其迁移能力。另外,Ezrin表达下调或降低Ezrin的Thr567磷酸化,能抑制PI3K、Akt及ERK的活性。以上结果提示,Ezrin活化激活PI3K/Akt与MAPK/ERK信号通路,对施旺细胞增殖和迁移能力具有促进作用。Schwann cells participate in the formation of myelin sheath and regeneration of impaired nerves.This is related to their ability to proliferate and migrate.The mechanism in which Ezrin regulates proliferation and migration of Schwann cell is still unclear.In the present study,Ezrin was knocked down or overexpressed in RSC96.Cell proliferation and migration were detected using qRT-PCR,MTT analysis,western blotting and cell scratch wound assay.The results indicated that down regulation of Ezrin expression can obviously inhibit RSC96 proliferation and migration.Ezrin overexpression had no effect on proliferation but improved migration of RSC96.In addition,phosphorylation of Thr567 of Ezrin was inhibited by Y27632,which led to the suppression of migration rather than proliferation of RSC96.Furthermore,down-regulation of Ezrin expression or reduction of Thr567 phosphorylation of Ezrin could inhibit the activities of PI3K,Akt and ERK.In conclusion,activation of Ezrin promotes proliferation and migration of Schwann cells via PI3K/Akt and MAPK/ERK signals.
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