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International Journal of Inflammation
Volume 2011, Article ID 351010, 7 pages
Research Article

Interleukin-1β Expression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells

1Institute of Zoology, National Taiwan University, 1 Roosevelt Road, Section 4, Taipei 106, Taiwan
2Department of Pediatrics and Pediatric Cardiology, Veterans General Hospital-Taipei, National Yang Ming University, Taipei 112, Taiwan
3Department of Life Science, National Taiwan University, Taipei 106, Taiwan

Received 15 March 2010; Revised 24 May 2010; Accepted 28 June 2010

Academic Editor: Ricardo Saban

Copyright © 2011 Chih-Hsin Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.