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miR-22 是血管光滑肌细胞表型调节和新密度形成的新媒介

Feng Yang^1,2, Qishan Chen¹, Shiping He²

¹Department of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China (F.Y., Q.C., M.Y., L.Z.).

|December 17, 2017

概括

微RNA-22 (miR-22) 调节血管光滑肌细胞 (VSMC) 的功能和新内的形成. 恢复miR-22水平为血管疾病提供了潜在的治疗方法,

科学领域:

分子生物学
心血管研究
基因调控

背景情况:

微RNA-22 (miR-22) 与血管光滑肌细胞 (VSMC) 的分化有关.
它在成熟的VSMC表型调节和新密度形成中的作用仍然很大程度上不明.
了解miR-22的目标和途径对于血管疾病研究至关重要.

研究的目的:

研究miR-22在VSMC表型调节和新密度形成中的作用.
在血管疾病中探索调节miR-22的治疗潜力.
确定参与VSMC功能的新型miR-22基因.

主要方法:

使用电线损伤小鼠模型,局部输送AgomiR-22或miR-22抑制剂.
在正常和患病的人类大腿动脉中检查miR-22表达.
在体内,体外和体内进行的VSMC表型切换研究.

主要成果:

miR-22过度表达增强了VSMC标记基因,抑制了增殖和迁移.
对 miR-22 的抑制产生了相反的效果;确定了 EVI1 为新的目标基因.
在受伤的动脉中,miR-22的过度表达减少了新密的形成,而抑制则增加了它.
在患病的人类动脉中发现了降低的miR-22和增加的MECP2/EVI1, 证实了反向关系.

结论:

miR- 22和EVI1是新兴的新型调节器,用于新内膜增生症的VSMC功能.
调节miR-22对血管疾病具有潜在的治疗策略.
这些发现为血管重塑的分子机制提供了新的见解.

关键词:

MDS1 和 EVI1 复杂位蛋白动脉样硬化细胞的移动细胞增殖甲基-CpG结合蛋白2 微RNAs 新亲密的

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