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BACE2缺乏会损害大脑内皮细胞内皮氧化合成酶的表达和功能

Tongrong He¹, Livius V d'Uscio¹, Zvonimir S Katusic¹

¹Departments of Anesthesiology and Perioperative Medicine, and Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota, USA.

Journal of neurochemistry

|August 7, 2023

概括

β位粉样蛋白前体蛋白 (APP) 分裂酶2 (BACE2) 在大脑血管中对内皮氧化合成酶 (eNOS) 的调节起着至关重要的作用. 减少BACE2的表达会损害氧化的产生,这表明BACE2是一种血管保护蛋白.

科学领域:

神经科学是一个神经科学.
血管生物学血管生物学
分子生物学分子生物学

背景情况:

贝塔位点粉样蛋白前体蛋白 (APP) 分裂酶2 (BACE2) 在脑血管内皮中表达高.
在阿尔茨海默氏症的脑血管内皮中,BACE2被下调.

研究的目的:

确定BACE2在内皮氧化合成酶 (eNOS) 的表达和功能中的作用.

主要方法:

用小干扰RNA (siRNA) 在人类大脑微血管内皮细胞 (BMECs) 中对BACE2进行基因下调.
腺病毒介导的APP的过度表达.
对下游分子目标的分析.
在BACE2缺乏的小鼠中评估内皮依赖放松和循环GMP产生.

主要成果:

BACE2下调降低了eNOS表达和氧化 (NO) 生产,增加了eNOS酸化在Thr495.
BACE2下调抑制了APP表达和可溶性APPα (sAPPα) 的产生.
APP过度表达和sAPPα治疗增强了eNOS表达.
确定了γ-氨基黄油酸B型受体亚单元1和克鲁佩尔样因子2作为下游目标.
在BACE2缺乏的小鼠中观察到受内皮依赖放松和循环GMP产生障碍.

结论:

BACE2 调节大脑血管中的 eNOS 表达和功能.
在大脑血管系统中,BACE2可能充当血管保护蛋白.
BACE2的调节失调会影响与阿尔茨海默病相关的血管功能.

关键词:

这就是为什么APP APP APP APP 阿尔茨海默氏症的疾病是阿尔茨海默氏症.应用程序 17mermer 应用程序在BACE1中获得了BACE1学位.对于GABA来说,这是一个很好的选择.这是大脑微血管.

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