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目的探讨碱性成纤维细胞生长因子(basic fibroblastgrowth factor,bFGF)对人脐带静脉内皮细胞(human umbilicalvein endothelial cells,HUVECs)内游离镁离子浓度([Mg2+]i)的调节机制研究。方法我们采用荧光指示剂mag-fura-2,运用PTi阳离子测定系统动态测HUVECs的[Mg2+]i。结果经酪氨酸激酶阻断剂(tyrphostin A23和genistein)、3-磷脂酰肌醇激酶阻断剂(wortmannin和LY294002)、磷脂酶Cγ阻断剂(U73122)预处理,能阻断bF-GF诱导的[Mg2+]i增加。但经磷脂酶Cγ阻断剂无活性的类似物(U73343)和丝裂原活化蛋白激酶阻断剂(SB202190和PD98059)预处理,不能阻断bFGF诱导的[Mg2+]i增加。结论bFGF通过酪氨酸激酶/3-磷脂酰肌醇激酶/磷脂酶Cγ信号传递途径使细胞内的Mg2+库释放Mg2+,从而增加HUVECs的[Mg2+]i。
Objective To investigate the regulatory mechanism of basic fibroblast growth factor (bFGF) on the concentration of free magnesium ion ([Mg2 +] i) in human umbilicalvein endothelial cells (HUVECs). Methods We used the fluorescent indicator mag-fura-2 to measure the [Mg2 +] i of HUVECs dynamically using the PTi cation assay system. Results The pretreatment with tyrosine kinase inhibitors (tyrphostin A23 and genistein), 3-phosphatidylinositol kinase inhibitors (wortmannin and LY294002) and phospholipase Cγ antagonist (U73122) blocked bF-GF Induction of [Mg2 +] i increases. However, pretreatment with phospholipase C gamma blocker-inactive analogues (U73343) and mitogen-activated protein kinase blockers (SB202190 and PD98059) failed to block bFGF-induced increases in [Mg2 +] i. Conclusion bFGF can release Mg2 + from the intracellular Mg2 + via tyrosine kinase / 3-phosphatidylinositol kinase / phospholipase Cγ signaling pathway and increase [Mg2 +] i of HUVECs.