Astrocyte mitochondria in in vitro models of ischemia

There is growing evidence that preservation of mitochondrial respiratory function during cerebral ischemia-reperfusion predicts the ultimate extent of tissue injury. Because neurons are selectively vulnerable to ischemic injury, many studies have focused on neuronal mitochondrial dysfunction in isch...

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Bibliographic Details
Published in:Journal of bioenergetics and biomembranes 2004-08, Vol.36 (4), p.317-321
Main Authors: Dugan, Laura L, Kim-Han, Jeong-Sook
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Astrocytes - metabolism
Brain - metabolism
Brain Ischemia - metabolism
Cell Hypoxia
Cell Membrane Permeability
Cytochromes c - metabolism
Disease Models, Animal
Energy Metabolism
Humans
Ischemia
Membrane Potentials
Mitochondria
Mitochondria - metabolism
Mitochondrial Proteins - metabolism
Neuroprotective Agents - metabolism
Oxidative Stress
Reactive Oxygen Species - metabolism
Respiratory function
Signal Transduction
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Summary:There is growing evidence that preservation of mitochondrial respiratory function during cerebral ischemia-reperfusion predicts the ultimate extent of tissue injury. Because neurons are selectively vulnerable to ischemic injury, many studies have focused on neuronal mitochondrial dysfunction in ischemia. However, positron emission tomography (PET) studies in animals and humans suggest that non-neuronal cells such as astrocytes may also experience mitochondrial metabolic compromise that contributes to ischemic necrosis. Astrocytes carry out a number of functions that are critical to normal nervous system function, including uptake of neurotransmitters, regulation of pH and ion concentrations, and metabolic support of neurons. Mitochondria are important for many of these actions. We have used a cell culture model of stroke, oxygen-glucose deprivation (OGD), to study the response of astrocyte mitochondria to ischemia, and to evaluate how changes in astrocyte mitochondrial function might affect neuronal survival and recovery after ischemia.
ISSN:0145-479X
1573-6881
DOI:10.1023/B:JOBB.0000041761.61554.44