Estradiol regulates monocyte chemotactic protein-1 in human coronary artery smooth muscle cells: a mechanism for its antiatherogenic effect

Seli E., Selam B., Mor G., Kayisli U., Pehlivan T., Arici A.

MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY, cilt.8, sa.4, ss.296-301, 2001 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 8 Sayı: 4
  • Basım Tarihi: 2001
  • Doi Numarası: 10.1097/00042192-200107000-00013
  • Dergi Adı: MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.296-301
  • Anahtar Kelimeler: atherosclerosis, estrogen, vascular smooth muscle cells, MESSENGER-RNA EXPRESSION, VASCULAR INJURY RESPONSE, CHEMOATTRACTANT PROTEIN-1, HEART-DISEASE, ATHEROSCLEROTIC LESIONS, DEFICIENT MICE, ESTROGEN, MACROPHAGE, FIBROBLASTS, ABSENCE
  • Acıbadem Mehmet Ali Aydınlar Üniversitesi Adresli: Hayır

Özet

Objective: The protective effect of estrogen against early atherosclerosis in animal models is well documented, but the mechanisms responsible for this effect are not well understood. The earliest recognizable event in the pathogenesis of atherosclerosis is an increased recruitment of macrophages into the arterial subendothelium. Macrophages first play a protective role by removing low-density lipoproteins, but when the cholesterol is in excess, macrophages are converted into foam cells and form atheromas. Recent human and animal data indicate that the recruitment of macrophages to the arterial wall is mediated by monocyte chemotactic protein-1 (MCP-1). We hypothesized that one of the mechanisms of estrogen's protective effect against atherosclerosis may be the down-regulation of MCP-1 expression in the arterial wall.