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Journal of Korean Neurosurgical Society 1998;27(12): 1627-1634.
The Significance of Induction of Heat Shock Protein-70 and Glial Fibrillary Acidic Protein Messenger RNA by Delayed Postischemic Hyperthermia Following Transient Focal Ischemia.
Young Kim
Department of Neurosurgery, Ulsan University Hospital, College of Medicine, University of Ulsan, Ulsan, Korea.
ABSTRACT
The heat shock protein, especially 70 class(HSP-70) and glial fibrillary acidic protein have been postulated to participate either in the injury process or in adaptive or protective tissue responses after induction by injurious events. We studied to find out the relationships between the regional expression of message for heat shock protein and glial fibrillary acidic protein and cellular survival in the repetitive stress/injury model. Sixty minutes of transient middle cerebral artery occlusion was produced in rats by insertion of an intraluminal filament. Twenty-four hours after reperfusion, awaken rats were subjected to normothermic(37-38degreesC) or hyperthermic(40degreesC) temperature modulation for 3 hours in a heating chamber. At times of either 2 or 24 hours after temperature modulation, brains were examined for mRNA expression of heat shock protein and glial fibrillary acidic protein by dot blot method. Four regions of interest were chosen: fronto-cingulate, sensorimotor, and piriform-insular cortex; and caudoputamen. The analysis demonstrated that HSP-70 at 2 hours after temperature modulation was expressed at low levels in all groups. However, at 24 hours, HSP-70 mRNA expression was upregulated by hyperthermia alone in frontocingulate(penumbral) cortex, and to an equal degree by sham hyperthermia, ischemic normothermia and ischemic hyperthermia in regions of core-ischemia. Moreover, HSP-70 mRNA was expressed unevenly in the same territory of infarction. Ischemic stress induced marked glial fibrillary acidic protein expression in both penumbra and ischemic core regions; in contrast, hyperthermic stress failed to make any significant difference between animal groups. Consequently, these data suggest that heat shock protein and glial fibrillary acidic protein upregulation after stress/injury are unlikely to be involved in cellular survival and to reflect injury severity also.
Key Words: Focal ischemia; Hyperthermia; Heat shock protein; Glial fibrillary acidic protein rats
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