Polysialylation of NCAM is upregulated by hyperthermia and participates in heat shock preconditioning-induced neuroprotection.
Neurobiol Dis
; 26(2): 385-95, 2007 May.
Article
de En
| MEDLINE
| ID: mdl-17336079
ABSTRACT
"Brain tolerance"--a phenomenon in which a subtoxic challenge confers resistance to subsequent brain injuries--provides an ideal opportunity for investigating endogenous neuroprotective mechanisms. We investigated the potential role of the polysialylated (PSA) form of neural cell adhesion molecule (NCAM), which is thought to play a key role in plasticity. In a model where prior exposure to heat shock protects against kainate-induced cell damage in the hippocampus, we show that hyperthermia upregulates PSA-NCAM expression for at least 1 week, without affecting neurogenesis. Pharmacological manipulation of heat shock protein (HSP) expression demonstrates a tight positive link between HSP70 and PSA-NCAM. Finally, the presence of PSA was functionally linked to brain tolerance, as protection against kainate-induced cell death by heat shock pre-exposure was abolished in the absence of NCAM polysialylation. The upregulation of PSA-NCAM by hyperthermia may have a significant impact on hippocampal plasticity, permitting induction of the complex molecular cascade responsible for neuroprotection.
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Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Acides sialiques
/
Souffrance cérébrale chronique
/
Réaction de choc thermique
/
Cytoprotection
/
Molécule d'adhérence cellulaire neurale L-1
/
Fièvre
/
Hippocampe
Type d'étude:
Prognostic_studies
Limites:
Animals
Langue:
En
Journal:
Neurobiol Dis
Sujet du journal:
NEUROLOGIA
Année:
2007
Type de document:
Article
Pays d'affiliation:
France