title: Basic fibroblast growth factor increases intracellular magnesium concentration through the specific signaling pathways.
abstract: Basic fibroblast growth factor (bFGF) plays an important role in angiogenesis. However, the underlying mechanisms are not clear. Mg(2+) 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 Mg(2+) concentration ([Mg(2+)](i)) in human umbilical vein endothelial cells (HUVECs). bFGF increased [Mg(2+)](i) in a dose-dependent manner, independent of extracellular Mg(2+). This bFGF-induced [Mg(2+)](i) increase was blocked by tyrosine kinase inhibitors (tyrphostin A-23 and genistein), phosphatidylinositol 3-kinase (PI3K) inhibitors (wortmannin and LY294002) and a phospholipase Cgamma (PLCgamma) inhibitor (U73122). In contrast, mitogen-activated protein kinase inhibitors (SB202190 and PD98059) did not affect the bFGF-induced [Mg(2+)](i) increase. These results suggest that bFGF increases the [Mg(2+)](i) from the intracellular Mg(2+) stores through the tyrosine kinase/PI3K/PLCgamma-dependent signaling pathways.
authors.affiliation: Department of Pharmacology, Chonbuk National University Medical School, Jeonju 560-182, Korea.
authors.forename: Bing-Zhe
authors.initials: BZ
authors.lastname: Hong
authors.forename: Sun-Ah
authors.initials: SA
authors.lastname: Park
authors.forename: Han-Na
authors.initials: HN
authors.lastname: Kim
authors.forename: Tian-Ze
authors.initials: TZ
authors.lastname: Ma
authors.forename: Han-Gyu
authors.initials: HG
authors.lastname: Kim
authors.forename: Hyung-Sub
authors.initials: HS
authors.lastname: Kang
authors.forename: Hwan-Gyu
authors.initials: HG
authors.lastname: Kim
authors.forename: Yong-Geun
authors.initials: YG
authors.lastname: Kwak
mesh_terms: D000730:Androstadienes / Q000494:pharmacology; D002460:Cell Line; D002867:Chromones / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D004963:Estrenes / Q000494:pharmacology; D016222:Fibroblast Growth Factor 2 / Q000494:pharmacology*; D005419:Flavonoids / Q000494:pharmacology; D019833:Genistein / Q000494:pharmacology; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D042541:Intracellular Space / Q000187:drug effects / Q000378:metabolism; D008274:Magnesium / Q000378:metabolism*; D008856:Microscopy, Fluorescence / Q000379:methods; D009025:Morpholines / Q000494:pharmacology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051966:Phospholipase C gamma / Q000037:antagonists & inhibitors / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors; D011725:Pyridines / Q000494:pharmacology; D011760:Pyrrolidinones / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects*; D020032:Tyrphostins / Q000494:pharmacology; D000077191:Wortmannin
chemical_list: D000730:Androstadienes; D002867:Chromones; D004963:Estrenes; D016222:Fibroblast Growth Factor 2; D005419:Flavonoids; D019833:Genistein; D007093:Imidazoles; D008274:Magnesium; D009025:Morpholines; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051966:Phospholipase C gamma; D047428:Protein Kinase Inhibitors; D011505:Protein-Tyrosine Kinases; D011725:Pyridines; D011760:Pyrrolidinones; D020032:Tyrphostins; D000077191:Wortmannin; C060229:1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; C090942:4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole; C060641:tyrphostin A23; C093973:2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one