tailieunhanh - Báo cáo khoa học: 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 estrogenreceptor independent

Dehydroepiandrosterone (DHEA), a steroid hormone, modified the proli-feration 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. . | ềFEBS Journal 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 Estrella Zapata1 Jose L. Ventura2 Karina De la Cruz3 Emma Rodriguez1 Pablo Damian3 Felipe Masso1 Luis F. Montano4 and Rebeca Lopez-Marure1 1 Departamento de Biologia Celular Institute Nacionalde Cardiologia Ignacio Chavez Mexico 2 Departamento de Biologia Celular Instituto de Fisiologia Celular UNAM Mexico 3 Departamento de Biologia de la Reproduccion UAM-Iztapalapa Mexico 4 Laboratorio de Inmunologia Depto. Bioquimica Facultad de Medicina UNAM Mexico Keywords dehydroepiandrosterone TNF cell cycle proteins HUVEC proliferation Correspondence R. Lopez-Marure Departamento de Biologia Celular Instituto Nacionalde Cardiologia Ignacio Chavez Juan Badiano no. 1 Colonia Seccion 16 Tlalpan CP 14080 Mexico DF Mexico Fax 52 55 73 09 26 Tel 52 55 73 29 11 ext. 1337 E-mail rlmarure@ Received 17 November 2004 revised 23 December 2004 accepted 10 January 2005 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. doi .

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