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

作者：Martini A^*; Bruno R; Mazzulla S; Nocita A; Martino G

来源：Acta Physiologica, 2010, 198(4): 449-455.

DOI：10.1111/j.1748-1716.2009.02070.x

• angiotensin II
• HUVEC
• mibefradil
• verapamil
• voltage-operated calcium channels

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 m and either Efonidipine 10-5 m or Verapamil 10-5 m or Mibefradil 10-5 m or Wortmannin 10-6 m. The contribution of Ang II receptors was evaluated using PD123319 10-7 m and 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.

• 出版日期2010-4