Title : Essential role of PI-3K, ERKs and calcium signal pathways in nickel-induced VEGF expression.

Pub. Date : 2005 Nov

PMID : 16283513






8 Functional Relationships(s)
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1 Essential role of PI-3K, ERKs and calcium signal pathways in nickel-induced VEGF expression. Nickel vascular endothelial growth factor A Homo sapiens
2 Previous studies have revealed that nickel compounds can induce the expression of vascular endothelial growth factor (VEGF), which is a key mediator of angiogenesis both in physiological and pathologic conditions. Nickel vascular endothelial growth factor A Homo sapiens
3 Previous studies have revealed that nickel compounds can induce the expression of vascular endothelial growth factor (VEGF), which is a key mediator of angiogenesis both in physiological and pathologic conditions. Nickel vascular endothelial growth factor A Homo sapiens
4 In the present study, we investigated the potential roles of PI-3K, ERKs, p38 kinase and calcium signalling in VEGF induction by nickel in Cl 41 cells. Nickel vascular endothelial growth factor A Homo sapiens
5 Exposure of Cl 41 cells to nickel compounds led to VEGF induction in both time- and dose-dependent manners. Nickel vascular endothelial growth factor A Homo sapiens
6 Pre-treatment of Cl 41 cells with PI-3K inhibitor, wortmannin or Ly294002, resulted in a striking inhibition of VEGF induction by nickel compounds, implicating the role of PI-3K in the induction. Nickel vascular endothelial growth factor A Homo sapiens
7 Pre-treatment of Cl 41 cells with intracellular calcium chelator, but not calcium channel blocker, inhibited VEGF induction by nickel. Nickel vascular endothelial growth factor A Homo sapiens
8 Collectively these data demonstrate that PI-3K, ERKs and cytosolic calcium, but not p38 kinase, play essential roles in VEGF induction by nickel compounds. Nickel vascular endothelial growth factor A Homo sapiens