COLIA1调控小鼠神经细胞迁移在神经管畸形中的作用
黄天楚, 黄琬淇, 顾卉, 袁正伟中国医科大学附属盛京医院卫生部小儿先天畸形重点实验室, 沈阳 110004
收稿日期:
2020-12-14出版日期:
2021-11-30发布日期:
2021-11-04通讯作者:
顾卉E-mail:huier.99@hotmail.com作者简介:
黄天楚(1985-),男,助理实验师,本科.基金资助:
国家自然科学基金(81771595)关键词: Ⅰ型胶原蛋白α1, 神经管畸形, 细胞迁移, 上皮细胞间质转化
Abstract: Objective To explore the effect of collagen typeⅠα1(COLIA1) during neural tube closure in mice by regulating neurocyte migration. Methods The pathogenesis of neural tube defects (NTDs) induced by all-transretinoic acid (ATRA) was studied in mouse models. The expression of COLIA1 and epithelial mesenchymal transition (EMT) markers (E-cadherin, Snail, and Vimentin) were detected by western blotting. After COLIA1 was silenced in C17.2 neural stem cells, the regulatory effects of COLIA1 on the expression of E-cadherin, Snail, and Vimentin were detected by western blotting. The changes in the biological activities of cell migration were observed through Transwell and cell scratching experiments to explore the regulatory effects of COLIA1 on neurocyte cell migration. Results In ATRA-induced NTDs in mice, COLIA1 expression was down-regulated and the related EMT markers Snail and Vimentin were down-regulated, while E-cadherin was up-regulated. In C17.2 neural stem cells, when the expression of COLIA1 was silenced, the EMT markers were changed correspondingly:Snail and Vimentin were down-regulated, E-cadherin was up-regulated, and the migration ability of the cells was decreased. Conclusion COLIA1 inhibits NTD formation by affecting cell migration.
Key words: collagen typeⅠα1, neural tube defects, cell migration, epithelial mesenchymal transition
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