Interleukin-1β Expression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells
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 cell...
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doaj-d51b2174a197408e99fcb06a1edba7442020-11-24T22:10:29ZengHindawi LimitedInternational Journal of Inflammation2042-00992011-01-01201110.4061/2011/351010351010Interleukin-1β Expression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial CellsChih-Hsin Lin0JenHer Lu1Hsinyu Lee2Institute of Zoology, National Taiwan University, 1 Roosevelt Road, Section 4, Taipei 106, TaiwanDepartment of Pediatrics and Pediatric Cardiology, Veterans General Hospital-Taipei, National Yang Ming University, Taipei 112, TaiwanInstitute of Zoology, National Taiwan University, 1 Roosevelt Road, Section 4, Taipei 106, TaiwanLysophosphatidic 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.http://dx.doi.org/10.4061/2011/351010 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Chih-Hsin Lin JenHer Lu Hsinyu Lee |
spellingShingle |
Chih-Hsin Lin JenHer Lu Hsinyu Lee Interleukin-1β Expression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells International Journal of Inflammation |
author_facet |
Chih-Hsin Lin JenHer Lu Hsinyu Lee |
author_sort |
Chih-Hsin Lin |
title |
Interleukin-1β Expression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells |
title_short |
Interleukin-1β Expression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells |
title_full |
Interleukin-1β Expression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells |
title_fullStr |
Interleukin-1β Expression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells |
title_full_unstemmed |
Interleukin-1β Expression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells |
title_sort |
interleukin-1β expression is required for lysophosphatidic acid-induced lymphangiogenesis in human umbilical vein endothelial cells |
publisher |
Hindawi Limited |
series |
International Journal of Inflammation |
issn |
2042-0099 |
publishDate |
2011-01-01 |
description |
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. |
url |
http://dx.doi.org/10.4061/2011/351010 |
work_keys_str_mv |
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