It has been shown by immunohistochemical studies that αB-crystallin accumulates in the reactive and neoplastic glial cells in a variety of pathologic situations. However, the molecular mechanism for the induction of αB-crystallin in diseased brains is still unknown. Since any destructive brain lesions cause an abnormal elevation in the potassium (K+) concentration of the extracellular space, which disturbs the regulatory mechanism of glial cell volume, we investigated the influence of elevated extracellular K+ on the expression of αB-crystallin in glial cells. The treatment of rat C6 glioma cells with augmented K+ in the culture media induced an accumulation of αB-crystallin mRNA in a dose-dependent manner and an accumulation of the αB-crystallin as well. Furthermore, an overexpression of αB-crystallin in the C6 transformant transfected with a rat αB-crystallin cDNA conferred a resistant phenotype against the insult of elevated extracellular K+ on the glioma cells. Thus, αB-crystallin may contribute to the survival of reactive glia in the presence of a high extracellular K+ concentration.
All Science Journal Classification (ASJC) codes
- General Neuroscience
- Molecular Biology
- Clinical Neurology
- Developmental Biology