Seli Emre, Pehlivan Tugce, Selam Belgin, Garcia-Velasco Juan A, Arici Aydin
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06520-8063, USA.
Fertil Steril. 2002 Mar;77(3):542-7. doi: 10.1016/s0015-0282(01)03223-x.
To determine whether estrogen down-regulates MCP-1 in vascular endothelial cells.
A prospective comparative study.
Academic research environment.
PATIENT(S): Human umbilical vein endothelial cells (n = 3) and human coronary artery endothelial cells (n = 3) obtained from females.
INTERVENTION(S): Human umbilical vein endothelial cells (HUVEC) and human coronary artery endothelial cells (HCAEC) were grown to preconfluence. Then, they were treated with various concentrations of estradiol (10(-11) M to 10(-7) M) as well as raloxifene (10(-7) M) and tamoxifen (10(-7) M). MCP-1 in culture media was quantified using an enzyme-linked immunosorbent assay (ELISA). Cellular ribonucleic acid (RNA) was extracted and Northern blots were hybridized with an oligonucleotide probe complementary to a specific sequence of MCP-1 mRNA.
MAIN OUTCOME MEASURE(S): MCP-1 protein and mRNA.
RESULT(S): Estrogen treatment did not change MCP-1 expression in HUVEC. On the other hand, in HCAEC, estradiol induced a 30% decrease in mRNA expression and resulted in dose-dependent inhibition of MCP-1 production as detected by ELISA. Raloxifene and tamoxifen also resulted in inhibition of MCP-1 mRNA and protein expression.
CONCLUSION(S): Our findings suggest that one of the mechanisms by which estrogen down-regulates atherosclerosis is by suppressing vascular MCP-1 expression, resulting in decreased macrophage recruitment.