Basic fibroblast growth factor (bFGF) plays an important role in angiogenesis. However, the underlying mechan-isms are not clear. Mg²⁺ is the most abundant intracellular divalent cation in the body and plays critical roles in many cell functions. We investigated the effect of bFGF on the intracellular Mg2+ concentration ([Mg²⁺]i) in human umbilical vein endothelial cells (HUVECs). bFGF increased [Mg²⁺]i in a dose-dependent manner, independent of extracellular Mg²⁺. This bFGF-induced [Mg²⁺]i increase was blocked by tyrosine kinase inhibitors (tyrphostin A-23 and genistein), phosphatidylinositol 3-kinase (PI3K) inhibitors (wortmannin and LY294002) or and a phospholipase C? (PLC?) inhibitor (U73122). In contrast, mitogen-activated protein kinase inhibitors (SB202190 and PD98059) did not affect the bFGF-induced [Mg²⁺]i increase. These results suggest that bFGF increases the [Mg²⁺]i from the intracellular Mg²⁺ stores through the tyrosine kinase/PI3K/PLCγ-dependent signaling pathways.

Keywords: angiogenesis, basic fibroblast growth factor, human umbilical vein endothelial cells, magnesium, signal transduction