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Previous studies demonstrated that calcium/calmodulin (Ca 2+ /CaM) activates nicotinamide adenine dinucleotide phosphate oxidases (NOX). In endothelial cells, the elevation of intracellular Ca 2+ level consists of two components: Ca 2+ mobilization from the endoplasmic reticulum (ER) and the subsequent store-operated Ca 2+ entry. However, little is known about which component of Ca 2+ increase is required to activate NOX in endothelial cells. Here, we investigated the mechanism that regulates NOX-derived reactive oxygen species (ROS) production via a Ca 2+ /CaM-dependent pathway.

Calcium Release from Endoplasmic Reticulum Involves Calmodulin-Mediated NADPH Oxidase-Derived Reactive Oxygen Species Production in Endothelial Cells