Hypoxia-ischemia induces heat shock protein-like (HSP72) immunoreactivity in neonatal rat brain.
The expression of heat shock protein immunoreactivity in rat brain was evaluated in a model of neonatal hypoxia-ischemia. One-week-old rats were subjected to left carotid artery coagulation and exposure to 8% O2/92% N2 for 2 h (moderate injury) or 3.5 h (severe injury). Animals were sacrificed 1, 12 and 24 h after the hypoxic insult. Cells immunoreactive for the 72 kDa heat shock protein (HSP72) were observed in ipsilateral cortex as early as 1 h after the termination of the hypoxia. After 12 h, neurons in the ipsilateral hippocampus and cortex stained intensely for HSP72 immunoreactivity in the moderately injured group. In the severely injured brains, bilateral staining was observed in neurons and vessels of the hippocampus and cortex. Therefore, cells containing HSP72 immunoreactivity may serve as an early marker for neuronal injury from hypoxia-ischemia in the neonatal rat brain and more importantly may illustrate previously unrecognized areas of central nervous system vulnerability.
Ferriero
D M
DM
Department of Neurology, University of California-San Francisco.
Soberano
H Q
HQ
Simon
R P
RP
Sharp
F R
FR
D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D002545:Brain Ischemia / Q000378:metabolism*; D005260:Female; D006360:Heat-Shock Proteins / Q000378:metabolism*; D002534:Hypoxia, Brain / Q000378:metabolism*; D007150:Immunohistochemistry; D051381:Rats; D011919:Rats, Inbred Strains
D006360:Heat-Shock Proteins