文章摘要
缺氧缺血诱导对原代新生大鼠前脑混合细胞髓鞘形成和细胞骨架的影响*
Effect of hypoxic-ischemic-induced on myelin formation and cytoskeleton of mixed forebrain cells in newborn rats*
投稿时间:2019-03-13  修订日期:2019-03-21
DOI:
中文关键词: 缺氧缺血诱导  髓鞘  细胞骨架  前脑混合细胞
英文关键词: Hypoxic-ischemic-induced  Myelination  Cytoskeleton  Mixed forebrain cells
基金项目:国家自然科学基金(批准号:81671496)
作者单位邮编
胡斌 陆军军医大学第二附属医院儿科 重庆 中国 400037
王成举 陆军军医大学第二附属医院儿科 重庆 中国 
杨望 陆军军医大学第二附属医院儿科 重庆 中国 
常琴 陆军军医大学第二附属医院儿科 重庆 中国 
屈福祥 陆军军医大学第二附属医院儿科 重庆 中国 
陈鹏慧 陆军军医大学基础医学院神经生物学教研室 重庆 中国 
张雨平* 陆军军医大学第二附属医院儿科 重庆 中国 400037
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中文摘要:
      目的:该研究探讨了缺氧缺血诱导对新生大鼠前脑混合细胞髓鞘形成和细胞骨架的影响。方法:在原代培养的新生大鼠前脑混合细胞中,应用免疫组化染色髓鞘碱性蛋白(MBP)和劳克坚牢蓝(LFB)染色检测髓鞘和轴突的发育情况;Western印迹分析NF155蛋白的表达情况;免疫荧光分析参与细胞骨架调节的ERM-Rho GTP酶家族相关蛋白表达。结果:缺氧缺血对混合细胞的进一步分化和成熟起到抑制作用,NF155和Rho GTP酶家族成员Rac1、Cdc42表达下降,细胞突起的形成和骨架重组受到阻碍,继而影响髓鞘的发育和成熟。结论:缺氧缺血造成髓鞘发育不良可能与ERM-Rho GTP酶细胞骨架通路受阻有关,NF155的减少亦可能是该通路受阻的原因之一。通过本实验,希望能为髓鞘相关性神经系统疾病寻求可能的新的损伤机制及干预途径。
英文摘要:
      Objective:The aim of this work was to investigate the effects of hypoxic ischemic on myelin formation and cytoskeleton of mixed forebrain cells in newborn rats. Methods:The expression of myelin development-related proteins myelin basic protein was verified by immunohistochemical staining and Luxol fast blue staining was used to detect the development of myelin sheath and axon in primary cultured mixed forebrain cells; the expression of protein NF155 was verified by Western blotting; the expression of ERM-Rho GTPase related proteins involved in cytoskeleton were verified by immunofluorescence analysis. Results:The results showed that hypoxic ischemic inhibited the further differentiation and maturation of mixed cells. The expressions of NF155, Rac1 and Cdc42 were decreased, and the formation of cell processes, the recombination of cytoskeleton were hindered, which affected the development and maturation of myelin sheath. Conclusions:In conclusion hypoxic-ischemic-induced the myelin dysplasia may be related to the obstruction of cytoskeleton network ERM-Rho GTPase signal pathway, and NF155 may be one of the reasons for the blockage of this pathway. It is hoped that this work will provide new ideas for the study of nervous system and solve the problem of myelin formation disorder.
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