Angiopoietin-1 increases intracellular free Mg2+ by tyrosine kinase/PI3K in HUVECs

AIM:The mechanism of angiopoietin-1 (Ang-1) in mediating increase in intracellular free magnesium (［Mg²⁺］_i) in human umbilical vein endothelial cells (HUVECs) was investigated in this study. METHODS:The change of ［Mg²⁺］_i in HUVECs was quantitatively detected in intracellular cation measurement system via loaded with the fluorescent magnesium indicator mag-fura-2. RESULTS:Ang-1 increased ［Mg²⁺］_i, and there was not any significant difference among the groups of 0 mmol/L and 1 mmol/L of extracellular Mg2+. Similar results were obtained in groups done with Ca2+. Pretreatment with tyrosine kinase inhibitors (tyrphostin A23 and genistein), phosphatidylinositol 3-kinase (PI3K) inhibitors (wortmannin and LY294002) blocked the increase in ［Mg²⁺］_i induced by Ang-1. However, mitogen-activated protein kinase inhibitors (SB202190 and PD98059) had no effect on the Ang-1-induced ［Mg²⁺］_iincrease. CONCLUSION:These results suggest that the increase in ［Mg²⁺］_i by Ang-1 come from intracellular Mg2+ pools mediated by tyrosine kinase/PI3K -dependent signaling pathways.