Journal
GLIA
Volume 63, Issue 6, Pages 1005-1020Publisher
WILEY-BLACKWELL
DOI: 10.1002/glia.22798
Keywords
leukemia inhibitory factor; galanin; oligodendrocytes
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Funding
- National Health and Medical Research Council (NHMRC) of Australia [628856]
- US National Multiple Sclerosis Society [RG 3850A3/1]
- NHMRC [454581]
- NHMRC Centre for Research Excellence Grant [1001216]
- Medical Research Council
- Wellcome Trust
- Diabetes UK
- National Institute on Aging [AG10668]
- Victorian Government Operational Infrastructure Support Programme
- Diabetes UK [12/0004538] Funding Source: researchfish
- Medical Research Council [G0300028, G1000863] Funding Source: researchfish
- MRC [G1000863, G0300028] Funding Source: UKRI
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In order to further investigate the molecular mechanisms that regulate oligodendrocyte (OC) survival, we utilized microarrays to characterize changes in OC gene expression after exposure to the cytokines neurotrophin3, insulin, or leukemia inhibitory factor (LIF) in vitro. We identified and validated the induction and secretion of the neuropeptide galanin in OCs, specifically in response to LIF. We next established that galanin is an OC survival factor and showed that autocrine or paracrine galanin secretion mediates LIF-induced OC survival in vitro. We also revealed that galanin is up-regulated in OCs in the cuprizone model of central demyelination, and that oligodendroglial galanin expression is significantly regulated by endogenous LIF in this context. We also showed that knock-out of galanin reduces OC survival and exacerbates callosal demyelination in the cuprizone model. These findings suggest a potential role for the use of galanin agonists in the treatment of human demyelinating diseases. GLIA 2015;63:1005-1020
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