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Titolo:
Regulation of vascular endothelial growth factor (VEGF) gene transcriptionby estrogen receptors alpha and beta
Autore:
Mueller, MD; Vigne, JL; Minchenko, A; Lebovic, DI; Leitman, DC; Taylor, RN;
Indirizzi:
Univ Calif San Francisco, Ctr Reprod Endocrinol, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Thomas Jefferson Univ, Philadelphia, PA 19107 USA Thomas Jefferson Univ Philadelphia PA USA 19107 hiladelphia, PA 19107 USA
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 20, volume: 97, anno: 2000,
pagine: 10972 - 10977
SICI:
0027-8424(20000926)97:20<10972:ROVEGF>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGESTERONE RECEPTORS; PRIMATE ENDOMETRIUM; RESPONSIVE ELEMENT; FACTOR EXPRESSION; MENSTRUAL-CYCLE; HUMAN UTERUS; CELLS; ANGIOGENESIS; IDENTIFICATION; LOCALIZATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Taylor, RN Univ Calif San Francisco, Ctr Reprod Endocrinol, Dept Obstet Gynecol & Reprod Sci, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 94143 USA
Citazione:
M.D. Mueller et al., "Regulation of vascular endothelial growth factor (VEGF) gene transcriptionby estrogen receptors alpha and beta", P NAS US, 97(20), 2000, pp. 10972-10977

Abstract

Vascular endothelial growth factor (VEGF) mediates angiogenic activity in a variety of estrogen target tissues. To determine whether estrogen has a direct transcriptional effect on VEGF gene expression, we developed a model system by transiently transfecting human VEGF promoter-luciferase reporter constructs into primary human endometrial cells and into Ishikawa cells, derived from a well-differentiated human endometrial adenocarcinoma. In primary endometrial epithelial cells, treatment with 17 beta-estradiol (E-2) resulted in a 3.8-fold increase in luciferase activity. whereas a 3.2-fold induction was demonstrated for stromal cells. Our Ishikawa cells had less than100 functional estrogen receptors (ER)/cell and were therefore cotransfected with expression vectors encoding either the alpha- or the beta-form of the human ER. In cells cotransfected with ER alpha. E-2 induced 3.2-fold induction in VEGF-promoter luciferase activity. A 2.3-fold increase was observed in cells cotransfected with ER beta. Through specific deletions, the E-2response was restricted to a single 385-bp PvuII-SstI fragment in the 5' flanking DNA. Cotransfection of this upstream region with a DNA binding domain ER mutant, or site-directed mutagenesis of a variant ERE within this fragment, resulted in the loss of the E-2 response. Electromobility shift assays demonstrated that this same ERE sequence specifically binds estradiol-ERcomplexes. These studies demonstrate that E-2-regulated VEGF gene transcription requires a variant ERE located 1.5 kb upstream from the transcriptional start site. Site-directed mutagenesis of this ERE abrogated E-2-induced VEGF gene expression.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 13:41:46