GPER1/GPR30 Activation Improves Neuronal Survival Following Global Cerebral Ischemia Induced by Cardiac Arrest in Mice

Female sex steroids, particularly estrogens, contribute to the sexually dimorphic response observed in cerebral ischemic outcome, with females being relatively protected compared to males. Using a mouse model of cardiac arrest and cardiopulmonary resuscitation, we previously demonstrated that estrog...

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Bibliographic Details
Published in:Translational stroke research 2012-12, Vol.3 (4), p.500-507
Main Authors: Kosaka, Y., Quillinan, N., Bond, C. T., Traystman, R. J., Hurn, P. D., Herson, P. S.
Format: Article
Language:English
Subjects:
Biomedical and Life Sciences
Biomedicine
Body temperature
Cardiac arrest
Cardiology
Cardiopulmonary resuscitation
Catheters
CPR
Estrogens
Females
Hormone replacement therapy
Hypotheses
Ischemia
Laboratory animals
Neurology
Neurosciences
Neurosurgery
Original Article
Potassium
Vascular Surgery
Ventilation
Ventilators
Womens health
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Summary:Female sex steroids, particularly estrogens, contribute to the sexually dimorphic response observed in cerebral ischemic outcome, with females being relatively protected compared to males. Using a mouse model of cardiac arrest and cardiopulmonary resuscitation, we previously demonstrated that estrogen neuroprotection is mediated in part by the estrogen receptor β, with no involvement of estrogen receptor α. In this study, we examined the neuroprotective effect of the novel estrogen receptor, G protein-coupled estrogen receptor 1 (GPER1/GPR30). Male mice administered with the GPR30 agonist G1 exhibited significantly reduced neuronal injury in the hippocampal CA1 region and striatum. The magnitude of neuroprotection observed in G1-treated mice was indistinguishable from estrogen-treated mice, implicating GPR30 in estrogen neuroprotection. Real-time quantitative RT-PCR indicates that G1 treatment increases expression of the neuroprotective ion channel, small-conductance calcium-activated potassium channel 2. We conclude that GPR30 agonists show promise in reducing brain injury following global cerebral ischemia.
ISSN:1868-4483
1868-601X
DOI:10.1007/s12975-012-0211-8