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KMID : 0578320090280010013
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Molecules and Cells
2009 Volume.28 No. 1 p.13 ~ p.17
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Basic fibroblast growth factor increases intracellular magnesium concentration through the specific signaling pathways
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Hong Bing-Zhe
Park Sun-Ah
Kim Han-Na
Ma Tian-Ze
Kim Han-Gyu
Kang Hyung-Sub
Kim Hwan-Gyu
Kwak Yong-Geun
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Abstract
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Basic fibroblast growth factor (bFGF) plays an important role in angiogenesis. However, the underlying mechanisms 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) and a phospholipase Cγ (PLCγ) 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.
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KEYWORD
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angiogenesis, basic fibroblast growth factor, human umbilical vein endothelial cells, magnesium, signal transduction
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