Overexpression of human S100B exacerbates brain damage and periinfarct gliosis after permanent focal ischemia.

ABSTRACT:

Background and purpose

We have previously demonstrated that augmented and prolonged activation of astrocytes detrimentally influences both the subacute and chronic phases of cerebral ischemia. Furthermore, we have suggested that the astrocyte-derived protein S100B may be important in these pathogenic events. However, the causal relationship between S100B and exacerbation of brain damage in vivo remains to be elucidated.

Methods

Using transgenic mice overexpressing human S100B (Tg huS100B mice), we examined whether S100B plays a cardinal role in aggravation of brain damage after permanent middle cerebral artery occlusion (pMCAO).

Results

Tg huS100B mice had significantly larger infarct volumes and worse neurological deficits at any time point examined after pMCAO as co

SUBMITTER: Mori T 

PROVIDER: S-EPMC2665284 | biostudies-literature | 2008 Jul

REPOSITORIES: biostudies-literature