Journal
PATHOLOGY RESEARCH AND PRACTICE
Volume 208, Issue 2, Pages 82-88Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.prp.2011.11.008
Keywords
Sphingosine 1-phosphate; Endothelial cells; Lipopolysaccharide; Tumor necrosis factor-alpha
Categories
Funding
- Natural Science Foundation of China [30071201, 81170297]
- Program for Changjiang Scholars and Innovative Research Team (PCSIRT) in University [IRT0731]
- National Key Foundation for Basic Science Research of China [G2005CB522601]
Ask authors/readers for more resources
Sphingosine-l-phosphate (SIP) is a bioactive sophospholipid with various S1P receptor (S1PR) expression profiles in cells of different origin. S1PR1, R3 and - to a lesser extent - R2 were the main receptors expressed in most of endothelial cells (ECs). The balances in the expression and activation of S1PR1. R2 and R3 help to maintain the physiological functions of ECs. Reverse transcription-PCR and Western blotting were used to detect the mRNA transcript level and protein expression of S1PR. Endothelial barrier function was measured by transflux of tracer protein through endothelial monolayer. Human dermal microvascular ECs predominantly expressed S1PR1 and S1PR3. Lipopolysaccharide (LPS) or tumor necrosis factor-alpha (TNF-alpha) significantly upregulated S1PR2 mRNA and protein levels. The application of S1PR2 antagonist JTE-013 decreased the endothelial monolayer hyper-permeability response induced by LPS and TNF-alpha. Inflammatory mediators LPS and TNF-alpha induce S1PR2 expression in endothelium, suggesting that S1PR2 up-regulation may be involved in LPS and TNF-alpha elicited endothelial barrier dysfunction. (C) 2011 Elsevier GmbH. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available