Intact mitochondrial Ca²⁺ uniport is essential for agonist-induced activation of endothelial nitric oxide synthase (eNOS).

ABSTRACT: Mitochondrial Ca²⁺ uptake regulates diverse endothelial cell functions and has also been related to nitric oxide (NO^•) production. However, it is not entirely clear if the organelles support or counteract NO^• biosynthesis by taking up Ca²⁺. The objective of this study was to verify whether or not mitochondrial Ca²⁺ uptake influences Ca²⁺-triggered NO^• generation by endothelial NO^• synthase (eNOS) in an immortalized endothelial cell line (EA.hy926), respective primary human umbilical vein endothelial cells (HUVECs) and eNOS-RFP (red fluorescent protein) expressing human embryonic kidney (HEK293) cells. We used novel genetically encoded fluorescent NO^• probes, the geNOps, and Ca²⁺ se

SUBMITTER: Charoensin S 

PROVIDER: S-EPMC5381715 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature