INDUCTION OF HEME OXYGENASE-1 (HO-1) IN GLIA AFTER TRAUMATIC BRAIN INJURY

Citation
K. Fukuda et al., INDUCTION OF HEME OXYGENASE-1 (HO-1) IN GLIA AFTER TRAUMATIC BRAIN INJURY, Brain research, 736(1-2), 1996, pp. 68-75
Citations number
29
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
736
Issue
1-2
Year of publication
1996
Pages
68 - 75
Database
ISI
SICI code
0006-8993(1996)736:1-2<68:IOHO(I>2.0.ZU;2-O
Abstract
In this study we examined the induction of heme oxygenase-1 (HO-1) in glia in the traumatized rat brain. HO-1 was immunolocalized in fixed s ections of brain 3 h to 5 days after injury. Induction of this enzyme in astrocytes, microglia/macrophages, and oligodendrocytes was evaluat ed using immunofluorescent double labeling with monoclonal antibodies to glial fibrillary acidic protein, complement C3bi receptor, and myel in basic protein. Induction of HO-1 was apparent in the injured hemisp here and cerebellum as early as 24 h postinjury. The protein was likew ise noted in similar regions of the brain at 72 h postinjury but appea red to be more widespread in its distribution. At 5 days postinjury, t here was a notable decline in the degree of immunostaining for HO-1. H O-1 was typically induced in astrocytes in the cerebral cortex at the site of impact, in the deep cortical layers adjacent to the hemorrhagi c lesions, and in the hippocampus. HO-1 was induced in Bergmann glia i n the vermis of cerebellum. In addition, HO-1 was also induced in micr oglia/macrophages scattered throughout the ipsilateral cerebral cortex , cerebellum and subarachnoid space. These findings demonstrate prolon ged glial induction of HO-1 in the traumatized brain. Such a response may reflect a protective role of these cells against secondary insults including oxidative stress.