Galanin is an Autocrine Myelin and Oligodendrocyte Trophic Signal Induced by Leukemia Inhibitory Factor

被引：10

作者：

Gresle, Melissa M. ^{[1
,2
]}

Butzkueven, Helmut ^{[1
,2
]}

Perreau, Victoria M. ^{[3
]}

Jonas, Anna ^{[4
]}

Xiao, Junhua ^{[3
]}

Thiem, Stefan ^{[5
,6
]}

Holmes, Fiona E. ^{[7
]}

Doherty, William ^{[4
]}

Soo, Pik-Ying ^{[4
]}

Binder, Michele D. ^{[3
,4
]}

Akkermann, Rainer ^{[3
]}

Jokubaitis, Vilija G. ^{[1
,2
]}

Cate, Holly S. ^{[3
,4
]}

Marriott, Mark P. ^{[4
]}

Gundlach, Andrew L. ^{[3
,4
]}

Wynick, David ^{[7
]}

Kilpatrick, Trevor J. ^{[3
,4
]}

机构：

[1] Univ Melbourne, Royal Melbourne Hosp, Melbourne Brain Ctr, Parkville, Vic 3050, Australia

[2] Univ Melbourne, Dept Med, Parkville, Vic 3050, Australia

[3] Univ Melbourne, Dept Anat & Neurosci, Parkville, Vic 3050, Australia

[4] Florey Inst Neurosci & Mental Hlth, Parkville, Vic, Australia

[5] Walter & Eliza Hall Inst Med Res, Parkville, Vic, Australia

[6] Univ Melbourne, Dept Med Biol, Parkville, Vic 3050, Australia

[7] Univ Bristol, Sch Physiol & Pharmacol & Clin Sci, Bristol, Avon, England

来源：

GLIA | 2015年 / 63卷 / 06期

基金：

澳大利亚国家健康与医学研究理事会; 英国医学研究理事会; 英国惠康基金;

关键词：

leukemia inhibitory factor; galanin; oligodendrocytes; CENTRAL-NERVOUS-SYSTEM; CYTOKINE RECEPTORS; GROWTH-FACTOR; CELL-DEATH; DEMYELINATION; ACTIVATION; EXPRESSION; FAMILY; STAT3; DIFFERENTIATION;

D O I：

10.1002/glia.22798

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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

引用

页码：1005 / 1020

页数：16

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