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Social stress exacerbates stroke outcome by suppressing Bcl-2 expression
A C DeVries1, H D Joh, O Bernard
1Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. devries.14@osu.edu
Summary
Psychological stress significantly reduces neuroprotective bcl-2 expression after stroke in mice. This stress-induced vulnerability highlights a potential behavioral target for improving stroke outcomes.
Area of Science:
- Neuroscience
- Molecular Biology
- Stress Research
Background:
- Psychological stress is linked to disease onset, but its specific role in stroke outcome is unclear.
- Understanding stress mechanisms is crucial for explaining individual variations in stroke severity.
Purpose of the Study:
- To investigate how chronic social stress affects neuronal survival and bcl-2 expression following ischemic stroke.
- To identify the molecular pathways linking psychological stress to stroke-induced brain injury.
Main Methods:
- Male mice (C57BL/6) underwent chronic social intimidation before a controlled ischemic insult.
- Measured bcl-2 messenger RNA (mRNA) expression and neuronal cell loss post-ischemia.
- Compared wild-type mice with transgenic mice overexpressing neuronal bcl-2.
Main Results:
- Stressed mice showed a 70% reduction in bcl-2 mRNA levels compared to unstressed controls.
- Social stress significantly worsened stroke-induced brain infarcts in wild-type mice.
- Enhanced bcl-2 expression in transgenic mice protected against stress-induced exacerbation of infarct size.
Conclusions:
- Chronic psychological stress impairs the brain's endogenous neuroprotective mechanisms, specifically bcl-2 expression, after ischemic injury.
- Elevated corticosterone levels correlated with larger infarcts in wild-type mice but not in bcl-2 transgenic mice.
- Targeting stress-induced molecular changes offers a novel therapeutic strategy for stroke treatment.