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[Apoptosis of astroglial cells]
1Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, Japan.
Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
|April 6, 1999
Summary
Astrocytes experience delayed cell death after calcium depletion and reperfusion, a process mediated by the sodium-calcium exchanger. Oxidative stress from hydrogen peroxide also induces astrocyte apoptosis, suggesting these glial cells are targets in brain injury.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Context:
- Astrocytes, the most prevalent glial cells in the brain, play crucial roles in both normal neuronal function and pathological conditions.
- Ischemia/reperfusion injury in the brain involves paradoxical changes in extracellular calcium, making astrocyte responses relevant to understanding brain damage.
Purpose:
- To investigate the mechanisms of astrocyte cell death following calcium depletion and reperfusion.
- To explore the role of oxidative stress and reactive oxygen species (ROS) in astrocyte injury and apoptosis.
Summary:
- Reperfusion of cultured astrocytes after calcium depletion induces delayed cell death, termed calcium paradox injury, mediated by the reverse mode of the sodium-calcium exchanger.
- Hydrogen peroxide exposure causes oxidative stress, leading to astrocyte DNA fragmentation and nuclear condensation, indicative of apoptosis.
- Protective effects were observed with heat shock proteins, glutathione, calcineurin inhibitors, NF-kappa B inhibitors, and caspase 3 inhibitors, suggesting multiple pathways involved in astrocyte survival.
Impact:
- This study identifies astrocytes as targets of reactive oxygen species and elucidates the apoptotic pathway in oxidative stress-induced astrocyte death.
- Findings provide insights into the cellular mechanisms underlying brain injury during ischemia/reperfusion and oxidative stress.
- The study highlights potential therapeutic targets for protecting astrocytes in neurological disorders.