title: Estradiol down-regulates MCP-1 expression in human coronary artery endothelial cells.
abstract: OBJECTIVE
  To determine whether estrogen down-regulates MCP-1 in vascular endothelial cells.
  
  
  METHODS
  A prospective comparative study.
  
  
  METHODS
  Academic research environment.
  
  
  METHODS
  Human umbilical vein endothelial cells (n = 3) and human coronary artery endothelial cells (n = 3) obtained from females.
  
  
  METHODS
  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.
  
  
  METHODS
  MCP-1 protein and mRNA.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06520-8063, USA.
authors.forename: Emre
authors.initials: E
authors.lastname: Seli
authors.forename: Tugce
authors.initials: T
authors.lastname: Pehlivan
authors.forename: Belgin
authors.initials: B
authors.lastname: Selam
authors.forename: Juan A
authors.initials: JA
authors.lastname: Garcia-Velasco
authors.forename: Aydin
authors.initials: A
authors.lastname: Arici
mesh_terms: D015152:Blotting, Northern; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis* / Q000235:genetics; D003331:Coronary Vessels / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D015536:Down-Regulation / Q000187:drug effects; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism* / Q000502:physiology; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D008875:Middle Aged; D011446:Prospective Studies; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D020849:Raloxifene Hydrochloride / Q000494:pharmacology; D020845:Selective Estrogen Receptor Modulators / Q000494:pharmacology; D013629:Tamoxifen / Q000494:pharmacology; D014471:Umbilical Veins / Q000187:drug effects / Q000378:metabolism / Q000502:physiology
chemical_list: D018932:Chemokine CCL2; D012333:RNA, Messenger; D020845:Selective Estrogen Receptor Modulators; D013629:Tamoxifen; D020849:Raloxifene Hydrochloride; D004958:Estradiol