Two heme oxygenase (HO) proteins have been identified to date; HO-1, a stress-induced protein, and HO-2, a constitutively expressed isoform. Recently, it was demonstrated that HO-1 mRNA expression is increased following transient global ischemia. The present study examined the effects of global and focal ischemia on HO-1 and HO-2 protein, using immunocytochemistry. Following 20 min of ischemia (rat 4 vessel occlusion model with hypotension) and 6 h of recirculation, increased HO-I immunoreactivity was evident in hippocampal neurons. After 24 h of recirculation, HO-1 was observed in both hippocampal neurons and astroglial cells. By 72 h, expression was primarily glial and restricted to CA1 and CA3c. In addition to hippocampus, HO-1 was also evident in both neurons and glial in cerebral cortex and thalamus, and in striatal glial cells. Twenty-four hours following permanent focal ischemia, HO-1 immunoreactivity was observed in astroglial cells in the penumbra region surrounding the infarct. In contrast to HO-1, the pattern of HO-2 immunoreactivity was not altered following transient global or permanent focal ischemia. The increased expression of HO-1 following ischemia may confer protection against oxidative stress, but might also contribute to the subsequent neuronal degeneration.
|Number of pages||4|
|State||Published - Jun 7 1996|
Bibliographical noteFunding Information:
This project was supportedb y NIH grants AG05144 (JWG), NS 33773 (LCP) ES01247, ES03698 and ES04931 (MDM); NIH Clinical InvestigatorD evelop-ment Award NS01505 (LCP), the Kentucky affiliate of the AmericanH eartA ssociation( LCP) and the Burroughs Wellcome Fund (MDM). We are grateful to Suzanne Bono and Vimala Bondadaf or assistancew ith manuscript preparation.
- Bile pigments
- Carbon monoxide
- Cerebral ischemia
- Focal ischemia
- Heat shock proteins
ASJC Scopus subject areas
- Neuroscience (all)