Inhibition of calpain reduces oxidative stress and attenuates endothelial dysfunction in diabetes.

ABSTRACT:

Aims

The present study was to investigate the role of calpain in reactive oxygen species (ROS) production in endothelial cells and endothelium-dependent vascular dysfunction under experimental conditions of diabetes.

Methods and results

Exposure to high glucose activated calpain, induced apoptosis and reduced nitric oxide (NO) production without changing eNOS protein expression, its phosphorylation and dimers formation in primary human umbilical vein endothelial cells (HUVECs). These effects of high glucose correlated with intracellular ROS production and mitochondrial superoxide generation. Selectively scavenging mitochondrial superoxide increased NO production in high glucose-stimulated HUVECs. Inhibition of calpain using over-expression of calpastatin or pharmacological c

SUBMITTER: Chen B 

PROVIDER: S-EPMC4045988 | biostudies-literature | 2014 May

REPOSITORIES: biostudies-literature