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AMPK通过促进Rab14依赖的ADAM10细胞表面转位来促进人类大动脉内皮细胞中的ADAM10脱落活动

Chung Hee Baek¹, Hyosang Kim¹, Soo Young Moon²

¹Division of Nephrology, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.

Biochemical and biophysical research communications

|July 14, 2023

概括

氨酸单酸激活蛋白激酶 (AMPK) 激活促进ADAM10细胞表面转位和脱落活动. 这个过程涉及Rab14依赖的贩运,影响细胞表面受体调节.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
生物化学生物化学

背景情况:

ADAM10 (一种分解蛋白和金属蛋白酶10) 分裂细胞表面受体,但其转位机制尚不清楚.
ADAM10调节了像RAGE,TNFR1和TLR4这样的受体.

研究的目的:

研究AMPK在ADAM10转位和脱落活动中的作用.
为了阐明ADAM10细胞表面转位的机制.

主要方法:

使用培养的人类大动脉内皮细胞 (HAECs).
使用的AICAR (AMPK激活剂),GI 254023X (ADAM10抑制剂),化合物C (AMPK抑制剂),以及ADAM10,AMPKα1和Rab14的siRNA.
评估了ADAM10细胞表面转位和RAGE细胞外域脱落.

主要成果:

艾卡尔治疗增加了ADAM10细胞表面转位和RAGE脱落.
AMPK激活 (酸化) 与ADAM10活性增加相关.
抑制AMPK或Rab14可以阻止AICAR诱导的ADAM10转位和RAGE脱落.

结论:

AMPK的激活会诱导ADAM10的分离活动.
在HAEC中,AMPK通过Rab14依赖机制促进ADAM10细胞表面转位.

关键词:

一个解体蛋白和金属蛋白酶10.由AMP激活的蛋白质激酶激活的蛋白质激酶.细胞表面贩运细胞表面贩运拉布14 (Rab14) 是一个对于高级糖化终端产品的受体.

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