Dehydroepiandrosterone inhibits the proliferation of human umbilical vein endothelial cells by enhancing the expression of p53 and p21, restricting the phosphorylation of retinoblastoma protein, and is androgen- and estrogen-receptor independent.
FEBS J
; 272(6): 1343-53, 2005 Mar.
Article
en En
| MEDLINE
| ID: mdl-15752352
Dehydroepiandrosterone (DHEA), a steroid hormone, modified the proliferation of human umbilical vein endothelial cells in a dose-dependent manner. Its inactive sulfate ester (DHEA-S) and two of its metabolites -- estradiol and testosterone -- had no inhibitory effect at physiological concentrations. Antiproliferation was associated with arrest in the G1 phase of the cell cycle, but not with cell death, as evaluated by cleavage of poly(ADP-ribose) polymerase and exposure of phosphatidylserine. The effect was not blocked by inhibitors of androgen or estrogen receptors. DHEA diminished the levels of phosphorylated retinoblastoma protein and increased the expression of p53 and p21 mRNAs. These results show that DHEA inhibits endothelial cell proliferation by regulating cell cycle relevant proteins through a cytoplasmic steroid hormone-independent pathway.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Endotelio Vascular
/
Receptores de Estrógenos
/
Proteína p53 Supresora de Tumor
/
Proteína de Retinoblastoma
/
Deshidroepiandrosterona
/
Proteínas de Ciclo Celular
Límite:
Humans
Idioma:
En
Revista:
FEBS J
Asunto de la revista:
BIOQUIMICA
Año:
2005
Tipo del documento:
Article
País de afiliación:
México
Pais de publicación:
Reino Unido