Polysialylation of NCAM is upregulated by hyperthermia and participates in heat shock preconditioning-induced neuroprotection
| Autor: | V. Duveau, S. Arthaud, A. Rougier, G. Le Gal La Salle |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Hyperthermia
Male Plasticity Fever PSA-NCAM Neurotoxins Neural Cell Adhesion Molecule L1 Biology Polysialic acid Neuroprotection Hippocampus lcsh:RC321-571 Body Temperature Brain tolerance Heat shock protein medicine Animals HSP70 Heat-Shock Proteins Rats Wistar lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry Cell damage Neurons Cell Death Neurogenesis medicine.disease Hsp70 Rats Up-Regulation nervous system Neurology Cytoprotection Nerve Degeneration Sialic Acids Neural cell adhesion molecule Brain Damage Chronic Neuroscience Heat-Shock Response |
| Zdroj: | Neurobiology of Disease, Vol 26, Iss 2, Pp 385-395 (2007) |
| ISSN: | 0969-9961 |
| Popis: | “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. |
| Databáze: | OpenAIRE |
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