[The findings indicate that HSP70 expression is closely related to ischemic brain injury, and that HSP70 expression is not related to either breakdown of the blood-brain barrier or reactive axonal changes].
The relationship between the 70-kilodalton hear shock protein (HSP70), morphological changes in neurons, protein extravasation, and reactive axonal changes was evaluated in rats with fluid percussion injuries to the right side of the brain. (4.8-5.6 atm, 20 ms). From 1 hour to 2 weeks after injury (or sham injury), serial sections of the brains were immunostained with antibodies to HSP70, rat IgG, and 68-kilodalton neurofilament. Ischemic changes in neurons in the injured cortex were noted in samples taken from 6 to 48 hours after injury, and macroscopic hemorrhages were noted in the corpus callosum and external capsule. Reactive axonal swelling was observed in the brain stem in samples taken from 6 to 48 hours after injury. Immunostaining of HSP70 was positive in the injured cortex from 6 hours to 1 week after injury. Maximal immunostaining was observed by 48 hours after injury in the injured cortical layers II and III. The region of HSP70 expression at 24 and 48 hours postinjury was the same as the region of ischemic cell changes. There were discrepancies between the region of HSP70 expression and the regions of IgG immunoreactivity and reactive axonal changes. These findings indicate that HSP70 expression is closely related to ischemic brain injury, and that HSP70 expression is not related to either breakdown of the blood-brain barrier or reactive axonal changes.
Hoshino
S
S
Department of Neurosurgery, Nippon Medical School, Tokyo, Japan.
D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D018840:HSP70 Heat-Shock Proteins