Estradiol ameliorates the reduction in parvalbumin expression induced by ischemic brain injury.

Abstract

Estradiol plays a neuroprotective role against focal cerebral ischemia. Parvalbumin is an intracellular Ca(2+)-binding protein. It exerts a neuroprotective effect against cytotoxic Ca(2+) overload. This study investigated whether estradiol modulates parvalbumin expression in focal cerebral ischemia and glutamate-induced neuronal cell death. Adult female rats were ovariectomied and treated with vehicle or estradiol prior to middle cerebral artery occlusion (MCAO). The cerebral cortex was collected 24h after MCAO. A proteomics approach showed a decrease of parvalbumin in MCAO-operated animals, while estradiol prevented the MCAO-induced decrease in parvalbumin. Reverse transcription-PCR and Western blot analyses confirmed that estradiol treatment attenuated the MCAO-induced decrease in parvalbumin levels. The results of immunohistochemical staining showed that the number of parvalbumin-positive cells decreased in MCAO-operated animals, and estradiol prevented the MCAO-induced decrease in parvalbumin-positive cells. In cultured hippocampal cells, glutamate exposure raised the intracellular Ca(2+) concentration, while estradiol treatment attenuated this increase. Moreover, estradiol prevented the decrease in parvalbumin induced by glutamate toxicity. These findings suggest that estradiol exerts a neuroprotective effect by preventing the MCAO-induced decrease of parvalbumin and by regulating intracellular Ca(2+) levels.

• Authors: Phil-Ok Koh
• Journal: Neuroscience letters (Neurosci Lett) Vol. 574 Pg. 36-40 (Jun 27 2014) ISSN: 1872-7972 [Electronic] Ireland
• PMID: 24831183 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Chemical References

• Neuroprotective Agents
• Parvalbumins
• Glutamic Acid
• Estradiol
• Calcium

Topics

• Animals
• Calcium (metabolism)
• Cell Death
• Cell Line
• Estradiol (metabolism, pharmacology)
• Female
• Glutamic Acid (pharmacology)
• Hippocampus (metabolism, pathology)
• Infarction, Middle Cerebral Artery (complications)
• Ischemic Attack, Transient (etiology, metabolism, pathology)
• Mice
• Neurons (drug effects, pathology)
• Neuroprotective Agents (pharmacology)
• Ovariectomy
• Parvalbumins (metabolism)
• Rats, Sprague-Dawley