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目的:探讨血管生成素-1(Ang-1)对人脐静脉内皮细胞(HUVECs)内游离镁离子浓度([Mg2+]i)的调节机制。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:Ang-1诱导的[Mg2+]i增加与细胞外Mg2+浓度无关。Ang-1诱导的[Mg2+]i增加与细胞内Ca2+浓度无关。经酪氨酸激酶阻断剂(tyrphostin A23和genistein),磷脂酰3激酶阻断剂(wortmannin和LY294002)预处理,均显著阻断Ang-1诱导的[Mg2+]i增加。但经活化丝裂原激活激酶阻断剂(SB202190和PD98059)预处理,不能阻断Ang-1诱导的[Mg2+]i增加。结论:Ang-1通过酪氨酸激酶/磷脂酰3激酶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 Ang-1 on free magnesium concentration ([Mg2 +] i) in human umbilical vein 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 increase of [Mg2 +] i induced by Ang-1 was independent of the extracellular Mg2 + concentration. Ang-1-induced [Mg 2+] i increase was independent of intracellular Ca 2+ concentration. Pretreatment with tyrosine kinase inhibitors (tyrphostin A23 and genistein) and phosphatidylinositol 3-kinase inhibitors (wortmannin and LY294002) significantly blocked the increase of [Mg2 +] i induced by Ang-1. However, pretreatment with activated mitogen-activated kinase inhibitors (SB202190 and PD98059) failed to block the increase in [Mg2 +] i induced by Ang-1. CONCLUSION: Ang-1 can release Mg2 + from intracellular Mg2 + via tyrosine kinase / phosphatidyl-3 kinase signaling pathway and increase [Mg2 +] i of HUVECs.