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Titolo:
Luteal angiogenesis: Prevention and intervention by treatment with vascular endothelial growth factor Trap(A40)
Autore:
Wulff, C; Wilson, H; Rudge, JS; Wiegand, SJ; Lunn, SF; Fraser, HM;
Indirizzi:
MRC, Human Reprod Sci Unit, Edinburgh EH3 9ET, Midlothian, Scotland MRC Edinburgh Midlothian Scotland EH3 9ET h EH3 9ET, Midlothian, Scotland Regeneron Pharmaceut Inc, Tarrytown, NY 10591 USA Regeneron Pharmaceut Inc Tarrytown NY USA 10591 , Tarrytown, NY 10591 USA
Titolo Testata:
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
fascicolo: 7, volume: 86, anno: 2001,
pagine: 3377 - 3386
SICI:
0021-972X(200107)86:7<3377:LAPAIB>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
MICROVASCULAR HYPERPERMEABILITY; MARMOSET MONKEY; CORPUS-LUTEUM; SOLID TUMORS; EXPRESSION; PRIMATE; ENDOMETRIOSIS; RECEPTOR; ANGIOPOIETIN-1; INHIBITION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Wulff, C MRC, Human Reprod Sci Unit, 37 Chalmers St, Edinburgh EH3 9ET, Midlothian,Scotland MRC 37 Chalmers St Edinburgh Midlothian Scotland EH3 9ET Scotland
Citazione:
C. Wulff et al., "Luteal angiogenesis: Prevention and intervention by treatment with vascular endothelial growth factor Trap(A40)", J CLIN END, 86(7), 2001, pp. 3377-3386

Abstract

The possibility of stimulating or inhibiting paracrine factors regulating angiogenesis may lead to new approaches for the treatment of pathological conditions of the female reproductive tract. We examined the effects of a clinical candidate, a soluble truncated form of the Flt-1 receptor, vascular endothelial growth factor trap(A40) (VEGF trap), in a primate model to determine its ability to prevent the onset of luteal angiogenesis or intervene with the on-going process. Marmosets were treated from the day of ovulationuntil luteal day 3 (prevention regimen) or on luteal day 3 for 1 day (intervention regimen). Effects of VEGF inhibition were studied by obtaining a proliferation index using bromodeoxyuridine incorporation, quantifying endothelial cell area using CD31, and assessing luteal function by plasma progesterone. After both treatments, intense luteal endothelial proliferation wassuppressed, a concomitant decrease in endothelial cell area confirmed the inhibition of vascular development, and a marked fall in plasma progesterone levels showed that luteal function was compromised. In, situ hybridization was used to localize and quantify compensatory effects on the expression of angiogenic genes. VEGF messenger ribonucleic acid (mRNA) expression in luteal cells was increased, whereas expression of its receptor, Fit, was decreased. inhibition of VEGF resulted in localized increased expression of angiopoietin-2 mRNA and its receptor, Tie-2. The results show that the VEGF trap can prevent luteal angiogenesis and inhibit the established process with resultant suppression of luteal function. Luteal Fit mRNA expression is dependent upon VEGF, and VEGF inhibition results in abortive increases in expression of VEGF, angiopoietin-2, and Tie-2.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 00:45:08