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Updated: Jul 10, 2026
On-Chip Endothelial Inflammatory Phenotyping
Published on: July 22, 2012
Estradiol reduces basal and cytokine induced monocyte adhesion to endothelial cells
Tomi S Mikkola1, Richard W St Clair
1Department of Pathology, Medical Center Boulevard, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Objective:
To investigate the effect of 17beta-estradiol (E2) on binding of monocytes to human aortic endothelial cells (HAECs) with or without cytokine induction.
Methods:
Confluent monolayers of HAECs were incubated with or without E2 for 48 h prior to the monocyte adhesion assay. In studies with cytokines, 1 ng/ml tumor necrosis factor-alpha (TNF-alpha), 20 U/ml interleukin-1beta (IL-1beta) or both were added to the culture medium for the final 24 or 4 h. For the measurement of monocyte adhesion, 3H-thymidine labeled human THP-1 monocytes (4 x 10(5) cells per well) were added to the confluent monolayer of HAECs and incubated at 37 degrees C for 90 min. The unbound THP-1 cells were removed by gentle washing, and bound cells were digested with NaOH and quantified by measuring radioactivity.
Results:
When HAECs were pretreated for 48 h with E2 the basal adhesion of THP-1 cells was reduced by an average of 28%. Estrogen significantly reduced cytokine-induced adhesion by 30-35% when the cytokines were added for 4 h. When the cytokine treatment was prolonged to 24 h, pretreatment of HAECs with E2 had no effect on THP-1 cell adhesion.
Conclusions:
E2 reduces basal and short-term cytokine induced monocyte binding to HAECs. Since monocyte adhesion to vascular endothelial cells is one of the initial steps in the pathogenesis of atherosclerosis, E2 may mediate vascular protection by reducing monocyte-endothelial cell binding in the early stages of atherogenesis.
