INV SUPERIOR JUBILADO
SEILICOVICH Adriana
artículos
Título:
Estradiol increases the Bax/Bcl-2 ratio and induces apoptosis in the anterior pituitary gland
Autor/es:
V. ZALDIVAR; M. L. MAGRI; S. ZARATE; G. JAITA; G. EIJO; D. RADL; J. FERRARIS; D. PISERA; A. SEILICOVICH
Revista:
NEUROENDOCRINOLOGY
Editorial:
KARGER
Referencias:
Año: 2009 vol. 90 p. 292 - 300
ISSN:
0028-3835
Resumen:
Background: Estrogens are recognized to act as modulators of pituitary cell renewal, sensitizing cells to mitogenic and apoptotic signals, thus participating in anterior pituitary (AP) homeostasis during the estrous cycle. The balance of pro and antiapoptotic proteins of the Bcl-2 family is known to regulate cell survival and apoptosis.
Aims: To understand the mechanisms underlying apoptosis during the estrous cycle, we evaluated the expression of the proapoptotic protein Bax and the antiapoptotic proteins Bcl-2 and Bcl-xL in the AP gland in cycling female rats, and the influence of estradiol on the expression of these proteins in AP cells of ovariectomized rats.
Methods/ Results: As determined by Western Blot, the expression of Bax was higher in AP glands from rats at proestrus than at diestrus I, Bcl-2 protein levels showed no difference and Bcl-xL expression was lower, thus increasing the Bax/Bcl-2 ratio at proestrus. Assessed by Annexin-V binding and flow cytometry, the percentage of apoptotic AP cells was higher in rats at proestrus than at diestrus I. Chronic estrogen treatment in ovariectomized rats, enhanced the Bax/Bcl-2 ratio and induced apoptosis. Moreover, incubation of cultured AP cells from ovariectomized rats with 17b-estradiol for 24 h increased the Bax/Bcl-2 ratio, decreased Bcl-xL expression and induced apoptosis.
Conclusion: Our results demonstrate that estradiol increases the ratio between proapoptotic and antiapoptotic proteins of the Bcl-2 family. This effect could participate in the sensitizing action of estrogens to proapoptotic stimuli and therefore be involved in the high apoptotic rate observed at proestrus in the AP gland.