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Gadolinium-promoted angiogenesis involves the activation of PKCα/β2 and MAPKs in human umbilical vein endothelial cells

Xiao Wan, Baodi Gou*, Kui Wang*   

  1. Department of Chemical Biology, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100191, China
  • Received:2012-08-08 Revised:2012-11-03 Online:2013-01-20 Published:2013-01-20
  • Contact: Baodi Gou*, Kui Wang*

Abstract: Gadolinium has been widely used as a contrast agent for magnetic resonance imaging in clinical practice. Recently, it was reported that gadolinium is involved in nephrogenic systemic fibrosis, although the exact mechanism by which gadolinium triggers nephrogenic systemic fibrosis remains unclear. In this study, we show that gadolinium chloride (GdCl3) induced human umbilical vein endothelial cells (HUVECs) to migrate in Matrigel and tubulogenesis during wound healing. Chick chorioallantoic membrane assay confirmed that GdCl3 stimulates angiogenesis. Under the optimal angiogenic concentration of GdCl3 (10 μM), intracellular calcium concentration and reactive oxygen species generation were elevated. Moreover, western blotting results indicate that in cells treated with GdCl3, Ca2+-dependent PKCα/β2 was phosphorylated, and MAPKs pathways were also activated. Taken together, GdCl3 has a potential effect on angiogenesis in HUVECs, and the possible mechanisms may involve oxidative stress and calcium-related signaling pathways.

Key words: Gadolinium chloride, Angiogenesis, Reactive oxygen species, Signaling pathways, Human umbilical vein endothelial cells

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