Interleukin-1βExpression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells
Author(s) -
ChihHsin Lin,
JenHer Lu,
Hsinyu Lee
Publication year - 2010
Publication title -
international journal of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.106
H-Index - 33
eISSN - 2090-8040
pISSN - 2042-0099
DOI - 10.4061/2011/351010
Subject(s) - lysophosphatidic acid , lymphangiogenesis , umbilical vein , vascular endothelial growth factor c , microbiology and biotechnology , proinflammatory cytokine , lymphatic endothelium , cytokine , inflammation , receptor , interleukin 8 , cancer research , lymphatic system , medicine , vascular endothelial growth factor a , biology , vascular endothelial growth factor , immunology , in vitro , biochemistry , vegf receptors , cancer , metastasis
Lysophosphatidic acid (LPA) is a lipid mediator which binds to G-protein-coupled receptors and regulates various cellular responses, including inflammation of endothelial cells. Interleukin- (IL-) 1β, a proinflammatory cytokine, is elevated upon LPA treatment in human umbilical vein endothelial cells (HUVECs). Previous studies indicated that LPA upregulates vascular endothelial growth factor- (VEGF-) C and lymphatic marker expressions in HUVECs. However, the relationships between LPA-induced VEGF-C and IL-1β expressions are not clear. In this paper, we demonstrated that, in the presence of AF12198, an inhibitor of the IL-1 receptor abolished LPA-induced VEGF-C and lymphatic marker expressions in HUVECs. Furthermore, LPA-induced in vitro tube formation of HUVECs was also suppressed by pretreatment with AF12198. Our results suggest that LPA-stimulated lymphangiogenesis in HUVECs is mediated through IL-1β-induced VEGF-C expression
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