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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Han, B.H. et al.

Clusterin contributes to caspase-3-independent brain injury following neonatal hypoxia-ischemia.

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.[1]

References

Clusterin contributes to caspase-3-independent brain injury following neonatal hypoxia-ischemia. Han, B.H., DeMattos, R.B., Dugan, L.L., Kim-Han, J.S., Brendza, R.P., Fryer, J.D., Kierson, M., Cirrito, J., Quick, K., Harmony, J.A., Aronow, B.J., Holtzman, D.M. Nat. Med. (2001) [Pubmed]

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