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Titolo:
Estradiol regulates monocyte chemotactic protein-1 in human coronary artery smooth muscle cells: a mechanism for its antiatherogenic effect
Autore:
Seli, E; Selam, B; Mor, G; Kayisli, UA; Pehlivan, T; Arici, A;
Indirizzi:
Yale Univ, Sch Med, Dept Obstet & Gynecol, New Haven, CT 06520 USA Yale Univ New Haven CT USA 06520 bstet & Gynecol, New Haven, CT 06520 USA
Titolo Testata:
MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY
fascicolo: 4, volume: 8, anno: 2001,
pagine: 296 - 301
SICI:
1072-3714(200107/08)8:4<296:ERMCPI>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RNA EXPRESSION; VASCULAR INJURY RESPONSE; CHEMOATTRACTANT PROTEIN-1; HEART-DISEASE; ATHEROSCLEROTIC LESIONS; DEFICIENT MICE; ESTROGEN; MACROPHAGE; FIBROBLASTS; ABSENCE;
Keywords:
atherosclerosis; estrogen; vascular smooth muscle cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Arici, A Yale Univ, Sch Med, Dept Obstet & Gynecol, 333 Cedar St, New Haven, CT 06520 USA Yale Univ 333 Cedar St New Haven CT USA 06520 Haven, CT 06520 USA
Citazione:
E. Seli et al., "Estradiol regulates monocyte chemotactic protein-1 in human coronary artery smooth muscle cells: a mechanism for its antiatherogenic effect", MENOPAUSE, 8(4), 2001, pp. 296-301

Abstract

Objective: The protective effect of estrogen against early atherosclerosisin 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 humanand 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. Design: Human coronary artery smooth muscle cells were replicated to confluence in smooth muscle cell basal medium supplemented with growth factors and 5% fetal bovine serum. Before each experiment, cells were incubated for 24 h with phenol red-free medium containing 5% charcoal-stripped calf serum, and then they were treated with various concentrations of 17 beta -estradiol as well as selective estrogen receptor (ER) modulators, raloxifene and tamoxifen. MCP-1 messenger ribonucleic acid (mRNA) levels were quantified by Northern blots. MCP-1 protein was quantified using an enzyme-linked immunosorbent assay. ER expression was evaluated by reverse transcriptase-polymerase chain reaction. Results: Human coronary artery smooth muscle cells expressed MCP-1 mRNA and produced MCP-1 protein. Estradiol induced up to 40% inhibition in mRNA expression at concentrations 10(-9) M and higher. Raloxifene and tamoxifen also resulted in an inhibition, but the inhibition was less than when inducedby estradiol. Estradiol also inhibited the MCP-1 protein production in a concentration-dependent manner (p < 0.05). Coronary smooth muscle cells expressed both ER alpha and ERP. Conclusion: Our findings suggest that one of the mechanisms by which estrogen prevents atherosclerosis is by down-regulating MCP-1 expression, thus decreasing macrophage recruitment to the arterial wail.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 16:34:53