Abstract
Objective
Reducing the expression of endothelial cell adhesion molecules (ECAMs) is known to decrease inflammation-induced vascular complications. In this paper we looked at whether statins can reduce inflammation-induced ECAM expression after lipopolysaccharide (LPS) treatment in endothelial cells.
Methods
Human umbilical vein endothelial cells (HUVECs) were pretreated with different concentrations of simvastatin, atorvastatin, and rosuvastatin and subsequently exposed to 5 μg/ml LPS. Semi-quantitative RT-PCR analysis was used to measure the mRNA expression of ECAMs, including VCAM-1, ICAM-1, and E-selectin.
Results
VCAM-1 mRNA appeared to be the only target that was affected by the statins, with its expression being partially and almost completely reduced by simvastatin at 50 and 125 μM concentrations, respectively, and only partially reduced by atorvastatin, but not reduced by rosuvastatin. VCAM-1 protein production was inhibited by simvastatin at concentrations from 5 to 125 μM. Leukocyte–endothelial cell adhesion assay revealed that simvastatin could inhibit the adhesion of labelled U937 cells to the HUVEC monolayer.
Conclusions
This study showed that simvastatin reduces VCAM-1 expression in HUVECs exposed to LPS and decreases leukocyte–endothelial cell adhesion.
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Abbreviations
- ECAMs:
-
Endothelial cell adhesion molecules
- VCAM-1:
-
Vascular cell adhesion molecule-1
- ICAM-1:
-
Intercellular cell adhesion molecule-1
- E-selectin:
-
Endothelial cell selectin
- HUVECs:
-
Human umbilical vein endothelial cells
- LPS:
-
Lipopolysaccharide
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Acknowledgments
The work was supported by the Chang Gung Memorial Hospital (CMRPG880511), Taiwan.
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Responsible Editor: Makoto Katori.
J.C.-S. Yang and F. Huang contributed equally to the work as the first author.
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Yang, J.CS., Huang, F., Wu, CJ. et al. Simvastatin reduces VCAM-1 expression in human umbilical vein endothelial cells exposed to lipopolysaccharide. Inflamm. Res. 61, 485–491 (2012). https://doi.org/10.1007/s00011-012-0435-9
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DOI: https://doi.org/10.1007/s00011-012-0435-9