Vascular endothelial growth factor increases the intracellular magnesium |
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Authors: | Hong Bing-Zhe Kang Hyung-Sub So June-No Kim Han-Na Park Sun-Ah Kim Shang-Jin Kim Kyung-Ryoul Kwak Yong-Geun |
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Institution: | Department of Pharmacology, Chonbuk National University Medical School, Jeonju, Jeonbuk 560-182, Republic of Korea. |
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Abstract: | Vascular endothelial growth factor (VEGF) is one of the key players in the process of angiogenesis. However, its underlying mechanism remains unclear. Mg2+ is the most abundant intracellular divalent cation in the body and plays critical roles in many cell functions. We investigated the effect of VEGF on intracellular Mg2+ in human umbilical vein endothelial cells (HUVECs). VEGF-A165 increased the intracellular Mg2+ concentration (Mg2+]i) in a dose-dependent manner, with or without extracellular Mg2+, and the increase of Mg2+]i was blocked by pretreatment with SU1498, tyrosine kinase inhibitors (tyrphostin A-23 and genistein), phosphatidylinositol 3-kinase (PI3K) inhibitors (wortmannin and LY294002) or phospholipase Cgamma (PLCgamma) inhibitor (U73122). In contrast, mitogen-activated protein kinase inhibitors (SB202190 and PD98059) had no effect on the VEGF-induced Mg2+]i increase. These results suggest that VEGF-A165 increases the Mg2+]i from the intracellular Mg2+ stores through the tyrosine kinase/PI3K/PLCgamma-dependent signaling pathways. |
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Keywords: | Vascular endothelial growth factors Signal transduction Magnesium Angiogenesis Human umbilical vein endothelial cells |
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