Astrocyte Mitochondria in In Vitro Models of Ischemia

Abstract

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.

Apoptosis: Future Targets for Neuroprotective Strategies

“…Ischemia-induced astrocytic death is blocked by caspase inhibitors [106]. Further details of this process are obtained from distinct paradigms demonstrating abnormal mitochondrial function of astrocytes in a cell culture model of stroke [107]. …”

Glial and Axonal Body Fluid Biomarkers Are Related to Infarct Volume, Severity, and Outcome

“…There is evidence that glial cells may be more susceptible to ischaemia than neurons. [2][3][4] Following cellular disintegration, cell-type specific proteins are released into the extracellular fluid (ECF). These proteins pass from the ECF into the cerebrospinal fluid (CSF) and blood, from where they can be quantified.…”

Astrocytes Role in Parkinson: A Double-Edged Sword

“…After brain damaging processes, neurons experience greater metabolic deterioration than glial cells. For instance, astrocytes contain glycogen stores that allow them to maintain ATP production through glycolysis and mitochondrial membrane potential by reversal of the F0-F1-ATPase (EC 3.6.3.14) [48]. For example, cultured astrocytes subjected to oxygen and glucose deprivation showed a decrease in mitochondrial membrane potential, possibly caused by the mitochondrial permeability transition pore (mtPTP) opening, which leads to a loss of intramitochondrial contents, mitochondrial respiration and ATP production [48].…”