Ovariectomy and 17 beta-estradiol replacement play a role on the expression of Endonuclease-G and phosphorylated cyclic AMP response element-binding (CREB) protein in hippocampus

Author(s)

dos Santos Pereira, Renato Tavares ^[1] ; Porto, Catarina Segreti ^[2] ; Francis Abdalla, Fernando Mauricio ^[1]

Affiliation

^[1] Inst Butantan, Pharmacol Lab, BR-05503900 Sao Paulo - Brazil

^[2] Univ Fed Sao Paulo, Escola Paulista Med, Dept Pharmacol, Sect Expt Endocrinol, Sao Paulo - Brazil

• Document type: Journal article
• Source: Molecular and Cellular Endocrinology; v. 382, n. 1, p. 227-233, JAN 25 2014.
• Web of Science Citations: 5

Abstract

The aim of the present study was to investigate the effects of different periods of ovariectomy and 17 beta-estradiol (E2) replacement on the expression of Cytochrome C, apoptosis inducing factor (AIF) and Endonuclease-G (Endo-G) in mitochondrial and cytosolic fractions obtained from hippocampus of the adult female rats. In addition, the expression of phosphorylated CREB (phospho-CREB) was also analyzed in hippocampus. Ovariectomy or E2 treatment did not change the expression of Cytochrome C and AIF. Ovariectomy (15, 21 and 36 days) decreased the expression of Endo-G in the mitochondrial fractions and increased it in the cytosolic fractions obtained from hippocampus. The treatment with E2 after 15 days of ovariectomy for 7 days or 21 days, and throughout the post-ovariectomy period prevented the effects of ovariectomy on Endo-G expression. Our results suggest that ovariectomy-induced apoptotic cell death in hippocampal tissue could be mediated by Endo-G, but not by AIF, via a caspase-independent apoptotic pathway. Furthermore, ovariectomy decreased the expression of phospho-CREB and the treatment with E2 prevented these effects. In conclusion, E2 may help maintain long-term neuronal viability by regulating the expression of members of the Bcl-2 family. Regulation of Endo-G released from mitochondria, but not of Cytochrome C and AIF, is also involved in the neuroprotective actions of E2. Furthermore, CREB may be involved in the expression of Bcl-2. These data provide new understanding into the mechanisms involved in the neuroprotective role of estrogen. (C) 2013 Elsevier Ireland Ltd. All rights reserved. (AU)

• FAPESP's process: 08/56564-1 - Estrogen receptors: expression, regulation, signaling, and function in the male reproductive tract, breast, and brain
• Grantee: Catarina Segreti Porto
• Support Opportunities: Research Projects - Thematic Grants