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Galanin is an autocrine myelin and oligodendrocyte trophic signal induced by leukemia inhibitory factor
Author(s) -
Gresle Melissa M.,
Butzkueven Helmut,
Perreau Victoria M.,
Jonas Anna,
Xiao Junhua,
Thiem Stefan,
Holmes Fiona E.,
Doherty William,
Soo PikYing,
Binder Michele D.,
Akkermann Rainer,
Jokubaitis Vilija G.,
Cate Holly S.,
Marriott Mark P.,
Gundlach Andrew L.,
Wynick David,
Kilpatrick Trevor J.
Publication year - 2015
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.22798
Subject(s) - galanin , leukemia inhibitory factor , autocrine signalling , paracrine signalling , biology , oligodendrocyte , neuropeptide , medicine , endocrinology , myelin , immunology , central nervous system , cytokine , receptor , interleukin 6 , biochemistry
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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