Send to

Choose Destination
Cell Calcium. 2001 Oct;30(4):235-44.

Calcium influx, arachidonic acid,and control of endothelial cell proliferation.

Author information

Department of Animal and Human Biology, University of Torino, Torino, Italy.


Recent evidences suggest a role for arachidonic acid (AA) in the triggering of store-independent, ornon-capacitative, calcium entry in different cell types. Here, using patch clamp and fluorimetric single-cell calcium measurements, we provide evidence for AA-activated calcium influx in bovine aortic endothelial cells (BAEC). AA-activated calcium entry is independent from intracellular calcium stores depletion at low doses of the fatty acid (< 5 microM) and insensitive to a decrease of pH to 6.7. Single-channel analysis in inside-out configuration reveals the presence of a family of AA-activated calcium-permeable channels, with different conductances and reversal potentials. Treatment with AA or ETYA induces a proliferative effect, significantly affected by external EGTA application during the early period (up to 2h) of stimulation with the agonists. We conclude that low concentrations of arachidonic acid are able to evoke a store-independent calcium influx, exerting a mitogenic role in BAECs.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center