Basic fibroblast growth factor increases intracellular magnesium concentration through the specific signaling pathways |
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Authors: | Bing-Zhe Hong Sun-Ah Park Han-Na Kim Tian-Ze Ma Han-Gyu Kim Hyung-Sub Kang Hwan-Gyu Kim Yong-Geun Kwak |
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Institution: | (1) Department of Transgenics, Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, LA 70808, USA;(2) Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610, USA |
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Abstract: | 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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