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Angiotensin II regulates endothelial cell migration through calcium influx via T-type calcium channel in human umbilical vein endothelial cells

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Abstract Aim: 

The T-type calcium channel is expressed in vascular endothelial cells, but its role in endothelial cell function is yet to be elucidated. We analysed the endothelial functional role of T-type calcium channel-dependent calcium under angiotensin II (Ang II) stimulation. Methods: 

Human umbilical vein endothelial cells were co-incubated with hormone at 10−7 mand either Efonidipine 10−5 mor Verapamil 10−5 mor Mibefradil 10−5 mor Wortmannin 10−6 m. The contribution of Ang II receptors was evaluated using PD123319 10−7 mand ZD 7155 10−7 m. The calcium ion concentration was observed using Fluo-3 acetossimetil ester. The cells were observed after 3, 6, 9 and 12 h. Results: 

The microfluorescence method points out that Ang II induces intracellular calcium modulation in time by distinct mechanisms. AT2 receptor blockade is necessary to observe significant increase in [Ca2+]i levels. Pre-treatment with Mibefradil abolishes Ang II -induced cell migration. Conclusions: 

Our data show that Ang II, via AT1 receptor, modulates calcium concentration involving T-type calcium channel and L-type calcium channel but only the calcium influx via T-type calcium channels regulates endothelial cell migration which is essential for angiogenesis.

Keywords: HUVEC; angiotensin II; mibefradil; verapamil; voltage-operated calcium channels

Document Type: Research Article


Affiliations:  Department of Cell Biology, Calabria University, Rende (CS), Italy

Publication date: April 1, 2010


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