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白细胞介素-1β的表达是溶血磷脂酸诱导人脐静脉内皮细胞淋巴管生成所必需的。

Interleukin-1β expression is required for lysophosphatidic Acid-induced lymphangiogenesis in human umbilical vein endothelial cells.

作者信息

Lin Chih-Hsin, Lu Jenher, Lee Hsinyu

机构信息

Institute of Zoology, National Taiwan University, 1 Roosevelt Road, Section 4, Taipei 106, Taiwan.

出版信息

Int J Inflam. 2010 Aug 4;2011:351010. doi: 10.4061/2011/351010.

DOI:10.4061/2011/351010
PMID:21151531
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2989649/
Abstract

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.

摘要

溶血磷脂酸（LPA）是一种脂质介质，它与G蛋白偶联受体结合并调节各种细胞反应，包括内皮细胞炎症。白细胞介素-（IL-）1β是一种促炎细胞因子，在人脐静脉内皮细胞（HUVECs）中经LPA处理后会升高。先前的研究表明，LPA上调HUVECs中血管内皮生长因子-（VEGF-）C和淋巴管标志物的表达。然而，LPA诱导的VEGF-C与IL-1β表达之间的关系尚不清楚。在本文中，我们证明，在存在IL-1受体抑制剂AF12198的情况下，可消除LPA诱导的HUVECs中VEGF-C和淋巴管标志物的表达。此外，用AF12198预处理也可抑制LPA诱导的HUVECs体外成管。我们的结果表明，LPA刺激HUVECs中的淋巴管生成是通过IL-1β诱导的VEGF-C表达介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/4ad867a1edbd/IJI2011-351010.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/ff26c804e167/IJI2011-351010.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/5f9b3e51256e/IJI2011-351010.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/78ee50c0e592/IJI2011-351010.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/4c8b56af12c3/IJI2011-351010.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/4ad867a1edbd/IJI2011-351010.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/ff26c804e167/IJI2011-351010.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/5f9b3e51256e/IJI2011-351010.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/78ee50c0e592/IJI2011-351010.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/4c8b56af12c3/IJI2011-351010.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bac7/2989649/4ad867a1edbd/IJI2011-351010.005.jpg

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