Activation of AMP-activated protein kinase inhibits oxidized LDL-triggered endoplasmic reticulum stress in vivo.

ABSTRACT:

Objective

The oxidation of LDLs is considered a key step in the development of atherosclerosis. How LDL oxidation contributes to atherosclerosis remains poorly defined. Here we report that oxidized and glycated LDL (HOG-LDL) causes aberrant endoplasmic reticulum (ER) stress and that the AMP-activated protein kinase (AMPK) suppressed HOG-LDL-triggered ER stress in vivo.

Research design and methods

ER stress markers, sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase (SERCA) activity and oxidation, and AMPK activity were monitored in cultured bovine aortic endothelial cells (BAECs) exposed to HOG-LDL or in isolated aortae from mice fed an atherogenic diet.

Results

Exposure of BAECs to clinically relevant concentrations of HOG-LDL induced prolonged ER stress and reduced SE

SUBMITTER: Dong Y 

PROVIDER: S-EPMC2874699 | biostudies-literature | 2010 Jun

REPOSITORIES: biostudies-literature