Inhibition of TNF-a induced ICAM-1, VCAM-1 and E-selectin expression by selenium

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Ethan W Taylor, Senior Research Professor (Creator)
The University of North Carolina at Greensboro (UNCG )
Web Site:

Abstract: The initiation of an atherosclerotic lesion involves an endothelial cell pro-inflammatory state that recruits leukocytes and promotes their movement across the endothelium. These processes require endothelial expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial-leukocyte adhesion molecule-1 (E-selectin). Tumor necrosis factor-a (TNF-a) is a powerful inducer of these adhesion molecules. Selenium status is known to affect the rate of atherosclerosis. These experiments tested whether selenium alters cytokine-induced expression of these adhesion molecules. Human umbilical vein endothelial cells (HUVECs) were pretreated for 24 h with sodium selenite (0–2 µM) and then treated with 0 or 50 U/ml TNF-a in the presence of 0–2 µM selenite. ICAM-1, VCAM-1 and E-selectin were detected by ELISA and their mRNAs were evaluated by Northern blots. Selenite significantly inhibited TNF-a-induced expression of each adhesion molecule in a dose-dependent manner and reduced the level of the respective mRNAs. Nuclear factor-kappaB (NF-kappaB) is required for transcription of these adhesion molecule genes. Western blot analysis revealed that selenite did not inhibit the translocation of the p65 subunit of NF-kappaB to the nucleus. In conclusion, these data indicate selenium can modulate cytokine-induced expression of ICAM-1, VCAM-1 and E-selectin in HUVECs without interfering with translocation of NF-kappaB.

Additional Information

Atherosclerosis. Volume 161, Issue 2, April 2002, Pages 381-386.
Language: English
Date: 2002
Selenium, ICAM-1, VCAM-1, E-selectin, NF-?B, HUVEC, Endothelium

Email this document to