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Titolo:
ESTROGEN INHIBITS THE RESPONSE-TO-INJURY IN A MOUSE CAROTID-ARTERY MODEL
Autore:
SULLIVAN TR; KARAS RH; ARONOVITZ M; FALLER GT; ZIAR JP; SMITH JJ; ODONNELL TF; MENDELSOHN ME;
Indirizzi:
TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,MOLEC CARDIOL RES CTR,750 WASHINGTON ST,BOX 80 BOSTON MA 02111 TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,MOLEC CARDIOL RES CTR BOSTON MA 02111 TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,DEPT MED,DIV CARDIOL BOSTON MA02111 TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,DEPT VASC SURG BOSTON MA 02111 TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,DEPT PATHOL BOSTON MA 02111
Titolo Testata:
The Journal of clinical investigation
fascicolo: 5, volume: 96, anno: 1995,
pagine: 2482 - 2488
SICI:
0021-9738(1995)96:5<2482:EITRIA>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
ATHEROSCLEROTIC CORONARY-ARTERIES; POSTMENOPAUSAL WOMEN; NITRIC-OXIDE; ESTRADIOL; DISEASE; THERAPY; PROLIFERATION; BIOSYNTHESIS; PROGESTERONE; COLLAGEN;
Keywords:
VASCULAR SMOOTH MUSCLE; ATHEROSCLEROSIS; STEROID HORMONES; C57BL/6J MICE; CAROTID ARTERY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
48
Recensione:
Indirizzi per estratti:
Citazione:
T.R. Sullivan et al., "ESTROGEN INHIBITS THE RESPONSE-TO-INJURY IN A MOUSE CAROTID-ARTERY MODEL", The Journal of clinical investigation, 96(5), 1995, pp. 2482-2488

Abstract

The atheroprotective effects of estrogen are well documented, but themechanisms responsible for these effects are not well understood. To study the role of physiologic (nanomolar) estrogen levels on the arterial response-to-injury, we applied a mouse carotid artery injury modelto ovariectomized C57BL/6J mice. Mice were treated with vehicle (-E2,n = 10) or 17 beta-estradiol (+E2, n = 10) for 7 d, subjected to unilateral carotid injury, and 14 d later contralateral (normal = NL) and injured carotids from -E2 and +E2 animals were pressure fixed, harvested, and analyzed by quantitative morphometry, E2 levels in +E2 mice were consistently in the nanomolar range (2.1-2.5 nM) at days 0, 7, and 14. At 14 d, measures of both intimal and medial area were markedly increased in the -E2 group: (-E2 vs NL, P < 0.05 for both), but were unchanged from normal levels in the +E2 group (+E2 vs NL, P = NS and +E2 vs -E2, P < 0.05 for both). Cellular proliferation, as assessed by bromodeoxyuridine (BrdU) labeling, was significantly increased over NL inthe -E2 mice, but this increase was markedly attenuated in the estrogen replacement group (total BrdU positive cells/section: NL = 6.4+/-4.5 -E2 = 113+/-26, +E2 = 40+/-3.7; -E2 vs NL, P < 0.05; +E2 vs NL, P = NS; -E2 vs +E2, P < 0.05). These data (a) demonstrate significant suppression of the mouse carotid response-to-injury by physiologic levels of estrogen replacement; (b) support the utility of this model in the study of the biologic effects of estrogen on the vascular-injury response; and (c) suggest a direct effect of estrogen on vascular smooth muscle cell proliferation in injured vessels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/10/20 alle ore 10:18:34