Abstract
Our previous study demonstrated that allograft inflammatory factor-1 (AIF-1) is present in the vessels of infantile hemangiomas but neither in the vessels of vascular malformations, pyogenic granulomas, normal skin, placental tissues nor in the neovessels of squamous cell carcinomas of the tongue. The purpose of this study was to explore the impact of AIF-1 alterations on endothelial cells (EC). Stable introduction of AIF-1 to the human umbilical vein EC line (HUV-EC-C) in vitro revealed that AIF-1 enhances the proliferation and migration of the EC and promotes G0/G1-to-S-phase transition, accompanied by up-regulation of basic fibroblast growth factor (p < 0.05). In contrast, AIF-1 did not affect the expression of granulocyte colony-stimulating factor, VEGF-a, monocyte chemoattractant protein-1, or tissue inhibitor of metalloproteinase-1. AIF-1 expression was not induced by hypoxia, VEGF-a, basic fibroblast growth factor, or insulin-like growth factor-2 in EC. Taken together, these findings suggest that the impact of AIF-1 on EC would stimulate angiogenesis and consequently affect the progression of infantile hemangiomas.
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Abbreviations
- AIF-1:
-
complementary allograft inflammatory factor-1
- bFGF:
-
basic fibroblast growth factor
- EC:
-
endothelial cell
- G-CSF:
-
granulocyte colony-stimulating factor
- hemEC:
-
hemangioma endothelial cell
- IH:
-
infantile hemangioma
- MAPK:
-
mitogen-activated protein kinase
- MCP-1:
-
monocyte chemoattractant protein-1
- PAK 1:
-
p21-activated kinases
- TIMP-1:
-
tissue inhibitor of metalloproteinase-1
- VSMC:
-
vascular smooth muscle cell
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Supported by Grant 20070486004 from the Ph.D. Programs Foundation of the Ministry of Education of China and by Grant NSFC 30872894 from National Natural Science Foundation of China (Y.-F.Z.).
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Jia, J., Cai, Y., Wang, R. et al. Overexpression of Allograft Inflammatory Factor-1 Promotes the Proliferation and Migration of Human Endothelial Cells (HUV-EC-C) Probably by Up-Regulation of Basic Fibroblast Growth Factor. Pediatr Res 67, 29–34 (2010). https://doi.org/10.1203/PDR.0b013e3181bf572b
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DOI: https://doi.org/10.1203/PDR.0b013e3181bf572b
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