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在高葡萄糖条件下,CCN1抑制会影响内皮原生细胞的功能

Yanting Dong^1,2, Xiaohui Zhou³, Nan Zhang¹

¹Department of Endocrinology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Advances in clinical and experimental medicine : official organ Wroclaw Medical University

|October 19, 2023

概括

高氨酸丰富的血管原生诱导剂61 (CCN1) 水平通过调节MEK/ERK通路,恢复糖尿病大鼠的内皮原生细胞 (EPC) 功能. 这一发现为糖尿病人血管修复提供了潜在的治疗策略.

科学领域:

内分泌学和新陈代谢学
细胞生物学细胞生物学
血管生物学血管生物学

背景情况:

在糖尿病大鼠的内皮原生细胞 (EPC) 中,富含氨酸的血管原生诱导剂61 (CCN1) 的作用尚不清楚.
在高葡萄糖 (HG) 条件下,在EPC中研究了CCN1,CXCR4和SDF-1的表达.

研究的目的:

探索CCN1升高对糖尿病大鼠EPC活性的影响.
研究MEK/ERK路径对CCN1和HG的反应的调制.

主要方法:

从链毒素诱导的糖尿病大鼠的骨髓和周围血液中分离出来的EPCs.
评估EPC迁移,生命力和管形成,使用跨孔,CCK-8和Matrigel测定.
通过西部斑块和RT-qPCR测量了蛋白质和基因表达.

主要成果:

高温条件降低了EPC的迁移,生存能力和管道形成.
高水平的CCN1通过在HG下诱导SDF-1和CXCR4恢复了EPC功能.
HG抑制了MEK/ERK酸化;一个ERK1/2激动剂通过MEK/ERK激活挽救了CCN1-SDF-1/CXCR4表达.

结论:

升高的CCN1恢复了EPC功能,部分是通过MEK/ERK信号.
这些发现支持糖尿病血管新生和修复的新疗法.

关键词:

CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CCN1 CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4CXCR4C 欧洲保险公司 (EPCs) 是一个欧洲保险公司.这就是SDF-1的特点.高葡萄糖的MEK/ERK信号通路.

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