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在糖尿病血管损伤中的功能障碍APPL1-介导表观遗传调节

Yunhui Du¹, Yanru Duan¹, Jianli Zhao²

¹Beijing Key Laboratory of Upper Airway Dysfunction-Related Cardiovascular Diseases, Beijing Institute of Heart, Lung, and Blood Vessel Diseases. Beijing Anzhen Hospital (Y. Du, Y. Duan), Capital Medical University, China.

Arteriosclerosis, thrombosis, and vascular biology

|October 5, 2023

概括

皮菌素 (APN) 和APPL1保护血管,但糖尿病会损害这种作用. APN恢复了APPL1的功能,抑制了HDAC2并促进了Angpt1,Ocln和Cav1等保护基因,这对于预防糖尿病血管损伤至关重要.

科学领域:

内分泌学在内分泌学.
分子生物学分子生物学
血管生物学血管生物学

背景情况:

阿迪波涅丁 (APN) 和APPL1对于血管健康至关重要,但它们的缺乏会导致糖尿病血管并发症.
通过APN和APPL1调节血管保护基因的精确分子机制以及糖尿病如何影响这些过程仍然不清楚.

研究的目的:

在糖尿病的背景下阐明APN和APPL1血管保护作用背后的分子机制.
为了确定由APN/APPL1调节的关键基因及其在糖尿病疾病中的改变.

主要方法:

使用糖尿病细胞模型 (老鼠和人类大动脉内皮细胞) 和体内模型 (糖尿病血管损伤,后肢缺血症).
研究了APN诱导的APPL1核转位,与HDAC2的相互作用,以及表观遗传修饰 (H3Kac27).
采用转录学,生物信息学,ChIP-qPCR和基因淘汰/淘汰策略来评估基因调节和功能结果.

主要成果:

APN的补充促进了APPL1的核转移,导致HDAC2的抑制和增加H3K27的乙化.
Angpt1,Ocln和Cav1被确定为关键的糖尿病抑制,APN救援的血管保护基因,由APN/APPL1.1调节.
在APN介导的途径中,Cav1在Angpt1/Ocln上游起作用,APN的保护作用取决于APPL1和Cav1,并被HDAC2.2抑制.

结论:

低基因染色体和受APPL1-介导的表观遗传调节中断是糖尿病诱导的血管保护性基因表达抑制的新贡献者.
促进APPL1核转位和抑制HDAC2的干预措施可以防止糖尿病诱导的病理血管重塑.

关键词:

没有任何的Adiponectin.血管新生素是一种血管新生素.洞穴里有洞穴,洞穴里有洞穴.饮食饮食饮食饮食血管系统损伤血管系统损伤

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