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Updated: Aug 14, 2026

Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions
Published on: August 23, 2013
Testosterone and estradiol modulate TNF-alpha-induced expression of adhesion molecules in endothelial cells
1Laboratory of Molecular Biology, Shanxi Medical University, Taiyuan, P.R. China.
Abstract:
Cytokine-activated endothelial expression of adhesion molecules plays an important role in immune responses. In the present study, we investigated the influences of testosterone and 17 beta-estradiol on tumor necrosis factor-alpha (TNF-alpha)-induced expression of adhesion molecules in human umbilical vein endothelial cells (HUVEC). HUVEC were incubated with TNF-alpha, testosterone or 17 beta-estradiol separately, or in a combination of TNF-alpha plus testosterone or 17 beta-estradiol. The expression of E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) was evaluated at 3, 6, 12 and 24 h following exposure by flow cytometric analysis. The results showed that although testosterone or 17 beta-estradiol did not affect the expression of these adhesion molecules in unstimulated HUVEC, both of them transiently increased the expression of E-selectin and VCAM-1 in TNF-alpha stimulated HUVEC. Neither testosterone nor 17 beta-estradiol affected the expression of ICAM-1 induced by TNF-alpha. It is concluded that both testosterone and 17 beta-estradiol increase TNF-alpha-induced expression of E-selectin and VCAM-1 in endothelial cells and these facts might indicate a mechanism by which gonadal hormones can indirectly enhance immune responses.
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