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长非编码RNA SNHG12在缺血性中风后通过RGMa调节勒普托门关节附带重塑

Anan Jiang¹, Zijie Wang¹, Ruiqi Cheng¹

¹Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

|August 13, 2024

概括

SNHG12促进血管光滑肌细胞 (VSMC) 不分化,并增强中风后的附带动脉生成. 向SNHG12可以通过调节SNHG12-MMP9信号和排斥引导分子a (RGMa) 来改善恢复.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
心血管研究研究心血管研究

背景情况:

勒普托门关节解瘤对于恢复脑血流 (CBF) 在缺血性中风后至关重要.
血管光滑肌细胞 (VSMC) 参与调节这种适应性反应,但机制尚不清楚.
长非编码RNA SNHG12在中风相关动脉生成过程中VSMC脱差中的作用尚不清楚.

研究的目的:

为了研究SNHG12在VSMC脱差和在缺血性中风后健康侧边动脉形成中的作用.
在这个过程中阐明涉及SNHG12,MMP9和RGMa的分子机制.

主要方法:

在VSMC脱差中研究了SNHG12表达和功能.
分析了SNHG12对MMP9和RGMa的影响.
评估了大脑血管封闭后对健康附带动脉发生的影响.

主要成果:

SNHG12作为MMP9和VSMC脱差的积极调节者.
SNHG12增强了脑血管封闭后的平侧动脉发生.
由RGMa介导的SNHG12-MMP9信号交叉声,限制了附带重塑.

结论:

在中风后,SNHG12促进VSMC脱差和附带动脉形成.
准SNHG12为中风恢复提供了一个潜在的治疗策略.
调节SNHG12可能会改善附带功能,神经健康和功能结果.

关键词:

缺血性中风是因为缺血性中风.莱普托马尼内尔额外担保改造在SNHG12中,SNHG12是SNHG12中的一个.

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