Estradiol prevents the injury-induced decrease of 90 ribosomal S6 kinase (p90RSK) and Bad phosphorylation.

Abstract

Estradiol prevents neuronal cell death through the activation of cell survival signals and the inhibition of apoptotic signals. This study investigated whether estradiol modulates the anti-apoptotic signal through the activation of Raf-MEK-ERK and its downstream targets, including 90 ribosomal S6 kinase (p90RSK) and Bad. Adult female rats were ovariectomied and treated with estradiol prior to middle cerebral artery occlusion (MCAO). Brains were collected 24h after MCAO and infarct volumes were analyzed. We confirmed that estradiol significantly reduces infarct volume and decreases the positive cells of TUNEL staining in the cerebral cortex. Estradiol prevents the injury-induced decrease of Raf-1, MEK1/2, and ERK1/2 phosphorylation. Also, it inhibits the injury-induced decrease of p90RSK and Bad phosphorylation. Further, in the presence of estradiol, the interaction of phospho-Bad and 14-3-3 increased, compared with that of oil-treated animals. Our findings suggest that estradiol prevents cell death due to brain injury and that Raf-MEK-ERK cascade activation and its downstream targets, p90RSK, Bad phosphorylation by estradiol mediated these protective effects.

• Authors: Phil Ok Koh
• Journal: Neuroscience letters (Neurosci Lett) Vol. 412 Issue 1 Pg. 68-72 (Jan 22 2007) ISSN: 0304-3940 [Print] Ireland
• PMID: 17196335 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• bcl-Associated Death Protein
• Estradiol
• Ribosomal Protein S6 Kinases, 90-kDa

Topics

• Animals
• Blotting, Western (methods)
• Brain Injuries (etiology, prevention & control)
• Enzyme Activation (drug effects)
• Estradiol (therapeutic use)
• Female
• Functional Laterality
• Infarction, Middle Cerebral Artery (complications)
• Ovariectomy (methods)
• Phosphorylation (drug effects)
• Rats
• Rats, Sprague-Dawley
• Ribosomal Protein S6 Kinases, 90-kDa (metabolism)
• bcl-Associated Death Protein (metabolism)