文章摘要
彭 浩,王义彪,刘朝晖,陈健龙,张 茂.miR-181c-5p在颅内动脉瘤中通过靶向PTPN4调节血管平滑肌细胞的机制研究[J].,2021,(12):2230-2234
miR-181c-5p在颅内动脉瘤中通过靶向PTPN4调节血管平滑肌细胞的机制研究
Study on the Mechanism of miR-181c-5p Regulating Vascular Smooth Muscle Cells by Targeting PTPN4 in Intracranial Aneurysms
投稿时间:2020-11-24  修订日期:2020-12-17
DOI:10.13241/j.cnki.pmb.2021.12.007
中文关键词: miR-181c-5p  血管平滑肌细胞  PTPN4  表型调节
英文关键词: miR-181c-5p  Vascular smooth muscle cells  PTPN4  Phenotypic modulation
基金项目:海南省2018年重点研发计划项目(ZDYF2018114)
作者单位E-mail
彭 浩 海南省人民医院/海南医学院附属海南医院神经外科 海南 海口 570000 haopenghaopenghp@163.com 
王义彪 海南省人民医院/海南医学院附属海南医院神经外科 海南 海口 570000  
刘朝晖 海南省人民医院/海南医学院附属海南医院神经外科 海南 海口 570000  
陈健龙 海南省人民医院/海南医学院附属海南医院神经外科 海南 海口 570000  
张 茂 海南省人民医院/海南医学院附属海南医院神经外科 海南 海口 570000  
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中文摘要:
      摘要 目的:探讨miR-181c-5p在颅内动脉瘤血管平滑肌细胞(VSMC)表型调节中的生物学功能及其潜在的调控机制。方法:采用实时荧光定量聚合酶链式反应(RT-qPCR)检测miR-181c-5p mRNA在颅内动脉瘤(IA)患者血清中的表达水平。 采用药物细胞毒性实验(CCK8)、集落形成、transwell迁移和流式细胞仪检测过表达miR-181c-5p介导的VSMC细胞表型的变化。采用双荧光素酶报告基因检测miR-181c-5p的潜在靶标。结果:IA患者血清中的miR-181c-5p表达水平高于健康体检者(P<0.05)。miR-181c-5p的过表达显着抑制了VSMC增殖、克隆形成和迁移,同时刺激了细胞凋亡(P<0.05)。PTPN4被证实是miR-181c-5p的直接靶标,而miR-181c-5p的过表达导致PTPN4在VSMC中低表达。结论:miR-181c-5p / PTPN4介导的VSMC表型调节可能部分导致IA病变。
英文摘要:
      ABSTRACT Objective: To investigate the biological function of miR-181c-5p in the phenotypic regulation of intracranial aneurysm vascular smooth muscle cells (VSMC) and its potential regulatory mechanism. Methods: Real time fluorescent quantitative polymerase chain reaction (RT-qPCR) was carried out to determine the miR-181c-5p and PTPN4 mRNA expression levels in serum of patients with intracranial aneurysm (IA). The changes overexpression of miR-181c-5p-mediated VSMC cell phenotypes were used to detect by cell counting Kit-8 (CCK8), colony formation, transwell migration and flow cytometry. Double luciferase reporter gene was performed to examine the potential target of miR-181c-5p. Results: The expression of miR-181c-5p in the serum of IA patients was higher than that of healthy subjects(P<0.05). The overexpression of miR-181c-5p significantly inhibited the proliferation, clone formation and migration of VSMC, and stimulated apoptosis (P<0.05). PTPN4 was proved to be a direct target of miR-181c-5p, and overexpression of miR-181c-5p resulted in low expression of PTPN4 in VSMC. Conclusion: miR-181c-5p/PTPN4-mediated VSMC phenotypic regulation may partially lead to IA lesions.
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