References
Query Results -- Details
MGI Accession ID: MGI:1931741
J Number: J:67960
Other Accession IDs:
Title: Clusterin contributes to caspase-3-independent brain injury following neonatal hypoxia-ischemia.
Authors: Han BH; DeMattos RB; Dugan LL; Kim-Han JS; Brendza RP; Fryer JD; Kierson M; Cirrito J; Quick K; Harmony JA; Aronow BJ; Holtzman DM
Journal: Nat Med
Volume: 7
Issue: 3
Date: 2001 Mar
Year: 2001
Pages: 338-43
Review Status: Peer Reviewed
Abstract:
Clusterin, also known as apolipoprotein J, is a ubiquitously expressed molecule thought to influence a variety of processes including cell death. In the brain, it accumulates in dying neurons following seizures and hypoxic-ischemic (H-I) injury. Despite this, in vivo evidence that clusterin directly influences cell death is lacking. Following neonatal H-I brain injury in mice (a model of cerebral palsy), there was evidence of apoptotic changes (neuronal caspase-3 activation), as well as accumulation of clusterin in dying neurons. Clusterin-deficient mice had 50% less brain injury following neonatal H-I. Surprisingly, the absence of clusterin had no effect on caspase-3 activation, and clusterin accumulation and caspase-3 activation did not colocalize to the same cells. Studies with cultured cortical neurons demonstrated that exogenous purified astrocyte-secreted clusterin exacerbated oxygen/glucose-deprivation-induced necrotic death. These results indicate that clusterin may be a new therapeutic target to modulate non-caspase-dependent neuronal death following acute brain injury.
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