VEGF165-induced angiogenesis by regulating intracellular free Mg2+ in HUVECs.
- Author:
Bing-Zhe HONG
1
;
Li-Ping WANG
;
Sheng-Fan LI
;
Hai-Nan PIAO
;
Li-Jian GAO
;
Wan-Qiu LI
;
Ping-An CAO
Author Information
- Publication Type:Journal Article
- MeSH: Cells, Cultured; Human Umbilical Vein Endothelial Cells; cytology; metabolism; physiology; Humans; Magnesium; metabolism; Neovascularization, Physiologic; drug effects; Phosphatidylinositol 3-Kinases; metabolism; Phospholipase C gamma; metabolism; Protein-Tyrosine Kinases; metabolism; Signal Transduction; Vascular Endothelial Growth Factor A; physiology
- From: Chinese Journal of Applied Physiology 2009;25(1):86-90
- CountryChina
- Language:Chinese
-
Abstract:
AIMThe mechanism of vascular endothelial growth factor165 (VEGF165) on intracellular free magnesium ([Mg2+]i) in human umbilical vein endothelial cells (HUVECs) was investigated.
METHODS[Mg2+]i in HUVECs loaded with fluorescent magnesium indicator mag-fura-2 were quantitatively detected the use of intracellular cation measurement system.
RESULTSVEGF165 significantly increased [Mg2+]i in the extracellular Mg2+ and this effect could be blocked by pretreatment with tyrosine kinase inhibitors (tyrphostin A23 and genistein), phosphatidylinositol 3-kinase (PI3K) inhibitors (wortmannin and LY294002) and phospholipase Cgamma (PLCgamma) inhibitor (U73122). In contrast, phospholipase Cgamma (PLCgamma) inhibitor analog (U73343), mitogen-activated protein kinase inhibitors (SB202190 and PD98059) had no effect on the VEGF165-induced [Mg2+]i increase.
CONCLUSIONThe increase of [Mg2+]i by VEGF165 originates from intracellular Mg2+ pool through tyrosine kinase/ PI3K/PLCgamma-dependent signaling pathways.
