Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 7-Day Trial for You or Your Team.

Learn More →

Lovastatin stimulates p75 TNF receptor (TNFR2) expression in primary human endothelial cells

Lovastatin stimulates p75 TNF receptor (TNFR2) expression in primary human endothelial cells HMG-CoA reductase inhibitors (statins) exert pleiotropic physiological effects. Among others they attenuate cellular responses to genotoxic and inflammatory stress. We investigated the effect of lovastatin on the expression level of TNF receptors (TNFR) in primary human endothelial cells (HUVEC). ELISA, FACS and immunocytochemical analyses show that lovastatin selectively increases the cell surface expression of TNFR2 without affecting the expression level of TNFR1. This effect of lovastatin is independent from inhibition of cell-cycle progression since cells both in G1- and G2-phase showed elevated levels of TNFR2 after lovastatin treatment. To analyze the physiological relevance of lovastatin-mediated upregulation of TNFR2, we investigated the expression of the cell adhesion molecule E-selectin, which is inducible by TNFα. While lovastatin on its own did not change the number of HUVEC expressing E-selectin protein, it promoted the TNFα-stimulated increase in the percentage of E-selectin expressing endothelial cells in a dose-dependent manner. This indicates that lovastatin sensitizes HUVEC towards TNFα-induced signaling by upregulation of TNFR2 expression. Based on the data, we suggest that statins have impact on endothelial responses to inflammatory stress by modulation of the expression of cytokine receptors. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png International Journal of Molecular Medicine Spandidos Publications

Lovastatin stimulates p75 TNF receptor (TNFR2) expression in primary human endothelial cells

Download PDF
7 pages

Loading next page...
 
/lp/spandidos-publications/lovastatin-stimulates-p75-tnf-receptor-tnfr2-expression-in-primary-bKBtR3UXKq

References

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Publisher
Spandidos Publications
Copyright
Copyright © Spandidos Publications
ISSN
1107-3756
eISSN
1791-244X
DOI
10.3892/ijmm.16.6.1139
Publisher site
See Article on Publisher Site

Abstract

HMG-CoA reductase inhibitors (statins) exert pleiotropic physiological effects. Among others they attenuate cellular responses to genotoxic and inflammatory stress. We investigated the effect of lovastatin on the expression level of TNF receptors (TNFR) in primary human endothelial cells (HUVEC). ELISA, FACS and immunocytochemical analyses show that lovastatin selectively increases the cell surface expression of TNFR2 without affecting the expression level of TNFR1. This effect of lovastatin is independent from inhibition of cell-cycle progression since cells both in G1- and G2-phase showed elevated levels of TNFR2 after lovastatin treatment. To analyze the physiological relevance of lovastatin-mediated upregulation of TNFR2, we investigated the expression of the cell adhesion molecule E-selectin, which is inducible by TNFα. While lovastatin on its own did not change the number of HUVEC expressing E-selectin protein, it promoted the TNFα-stimulated increase in the percentage of E-selectin expressing endothelial cells in a dose-dependent manner. This indicates that lovastatin sensitizes HUVEC towards TNFα-induced signaling by upregulation of TNFR2 expression. Based on the data, we suggest that statins have impact on endothelial responses to inflammatory stress by modulation of the expression of cytokine receptors.

Journal

International Journal of Molecular Medicine – Spandidos Publications

Published: Dec 1, 2005

There are no references for this article.