Literature DB >> 9272834

Marked alterations in the cellular localisation and levels of apolipoprotein E following acute subdural haematoma in rat.

K Horsburgh1, M Fitzpatrick, M Nilsen, J A Nicoll.   

Abstract

Apolipoprotein E (apoE) plays a role in the response to acute brain injury, the mechanisms as yet remain unknown. In the present study, alterations in the immunohistochemical localisation of apoE in rat cortex were examined at 30 min, 2 h or 4 h following production of an acute subdural haematoma. Levels of apoE were determined in cortex by immunoblotting at 30 min and 4 h post-haematoma. Extensive areas of ischaemic cell damage were observed in the cortex underlying the haematoma with minimal damage observed in shams. In sham animals, apoE immunoreactivity was confined to astrocytes and their processes. Following the haematoma induction, apoE immunoreactivity was dramatically altered. At 30 min post-haematoma, intense apoE staining was observed in clusters of neuronal perikarya and the neuropil throughout the cortical layers underlying the haematoma and this persisted at 2 h and 4 h post-haematoma. Additionally, at 4 h post-haematoma marked apoE staining of discrete foci within the neuropil closely associated with capillaries was consistently observed in the ipsilateral cortex. Immunoblotting indicated there were no significant alterations in the cortical levels of apoE at 30 min post-haematoma but, at 4 h post-haematoma, there was a significant elevation (27%, P < 0.001) in the levels of apoE in cortex underlying the haematoma compared to control levels. The results indicate that following acute subdural haematoma, a rapid cellular redistribution of apoE occurs and precedes a significant elevation in the levels of apoE. These alterations in apoE may occur, at least initially, as part of the brain's protective response to injury.

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Year:  1997        PMID: 9272834     DOI: 10.1016/s0006-8993(97)00411-3

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


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