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Regulation of noncapacitative calcium entry by arachidonic acid and nitric oxide in endothelial cells
Author(s) -
Mottola Annalisa,
Antoniotti Susanna,
Lovisolo Davide,
Munaron Luca
Publication year - 2005
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.05-4110fje
Subject(s) - microbiology and biotechnology , nitric oxide , calcium , arachidonic acid , calcium in biology , chemistry , endothelial stem cell , second messenger system , biology , biochemistry , intracellular , endocrinology , in vitro , enzyme , organic chemistry
Several peptides, including vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), activate the release of arachidonic acid (AA) and nitric oxide (NO) in endothelial cells (ECs). Both messengers are involved in EC proliferation and vascular permeability and control calcium homeostasis in different ways. Interestingly, it has been recently suggested that NO acts as a downstream mediator of AA‐induced calcium entry in smooth muscle cells and isolated mouse parotid cells. In this paper, we have investigated the complex relationships that link intracellular calcium, AA, and NO in cultured endothelial cells. Using different experimental approaches, mainly simultaneous Ca 2+ and NO fluorimetric confocal imaging, we provide evidence for a complex pathway leading to noncapacitative calcium entry (NCCE) in bovine aortic endothelial cells (BAECs). In particular, AA is able to induce NCCE through two different pathways: one dependent on eNOS recruitment and NO release, the other NO‐independent. Finally, we show that NO increase is involved in the control of BAEC proliferation.