Angiopoietin-1Increases Intracellular Free Mg²⁺ By Tyrosine Kinase/PI3K In HUVECs

Objective:The mechanism of Angiopoietin-1(Ang-1) in mediating increase of intracellular free magnesium ([Mg2+];) in human umbilical vein endothelial cells (HUVECs) were investigated in this study.Methods:The changes of [Mg2+]i in HUVECs were quantitatively detected in intracellular cation measurement system loaded with the fluorescent magnesium indicator mag-fura-2.Results:Ang-1increased [Mg2+]i, and there was not any significant difference among the groups of0mmol/L and1mmol/L of extracellular Mg2+; similar results were obtained in groups done with Ca2+。Pretreatment with tyrosine kinase inhibitors (tyrphostin A23and genistein), phosphatidylinositol3-kinase (PI3K) inhibitors (wortmannin and LY294002) blocked the increase of [Mg2+]i induced by Ang-1, mitogen-activated protein kinase inhibitors (SB202190and PD98059) had no effect on the Ang-1-induced [Mg2+]; increase.Conclusion:These results suggest that Ang-1increase [Mg2+]i via induced Mg2+release from intracellular Mg2+pools, which is mediated by tyrosine kinase/PI3K-dependent signaling pathways.