Insulin-Like Growth Factor (IGF) Signaling through Type 1 IGF Receptor Plays an Important Role in Remyelination

Mason, Jeffrey L.; Xuan, Shouhong; Dragatsis, Ioannis; Efstratiadis, Argiris; Goldman, James E.

doi:10.1523/jneurosci.23-20-07710.2003

Cited by 158 publications

(124 citation statements)

References 46 publications

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“…Although IGF-I reduces the loss of oligodendrocytes when transgenically overexpressed, mice lacking the IGF-I receptor within oligodendrocytes fail to show any acceleration in cuprizone-mediated loss of oligodendrocytes, displaying deficiencies confined to the subsequent remyelination phase (21,25). These findings, in combination with our observations that the loss of oligodendrocytes is exacerbated in LIF Ϫ/Ϫ mice, suggest that LIFR signaling is an important endogenous mechanism for limiting oligodendroglial injury and loss in vivo.…”

Section: Discussionsupporting

confidence: 55%

“…Although a number of cytokine systems influence the remyelination phase after cuprizone-mediated demyelination, including TNF-␣, IGF-I, FGF-2, and IL-1␤ (22)(23)(24)(25), less is known about the cytokines that modulate the initial loss of oligodendrocytes. Although IGF-I reduces the loss of oligodendrocytes when transgenically overexpressed, mice lacking the IGF-I receptor within oligodendrocytes fail to show any acceleration in cuprizone-mediated loss of oligodendrocytes, displaying deficiencies confined to the subsequent remyelination phase (21,25).…”

Section: Discussionmentioning

confidence: 99%

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Suppressor of cytokine signaling 3 limits protection of leukemia inhibitory factor receptor signaling against central demyelination

Emery

Cate

Marriott

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Enhancement of oligodendrocyte survival through activation of leukemia inhibitory factor receptor (LIFR) signaling is a candidate therapeutic strategy for demyelinating disease. However, in other cell types, LIFR signaling is under tight negative regulation by the intracellular protein suppressor of cytokine signaling 3 (SOCS3). We, therefore, postulated that deletion of the SOCS3 gene in oligodendrocytes would promote the beneficial effects of LIFR signaling in limiting demyelination. By studying wild-type and LIF-knockout mice, we established that SOCS3 expression by oligodendrocytes was induced by the demyelinative insult, that this induction depended on LIF, and that endogenously produced LIF was likely to be a key determinant of the CNS response to oligodendrocyte loss. Compared with wild-type controls, oligodendrocyte-specific SOCS3 conditional-knockout mice displayed enhanced c-fos activation and exogenous LIF-induced phosphorylation of signal transducer and activator of transcription 3. Moreover, these SOCS3-deficient mice were protected against cuprizone-induced oligodendrocyte loss relative to wild-type animals. These results indicate that modulation of SOCS3 expression could facilitate the endogenous response to CNS injury.oligodendrocyte ͉ SOCS3 ͉ cuprizone ͉ signal transduction ͉ conditional knockout

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Suppressor of cytokine signaling 3 limits protection of leukemia inhibitory factor receptor signaling against central demyelination

Emery

Cate

Marriott

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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“…Finally, late endosomes fuse with the lysosomal compartment (Tjelle et al (Mason et al 2003;Zeger et al 2007); Neuronal development (Schlueter et al 2007) ErbB4…”

Section: Endocytosis and Endosomal Targetingmentioning

confidence: 99%

Directing traffic in neural cells: determinants of receptor tyrosine kinase localization and cellular responses

Romanelli

Wood²

2008

Journal of Neurochemistry

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The trafficking of receptor tyrosine kinases (RTKs) to distinct subcellular locations is essential for the specificity and fidelity of signal transduction and biological responses. This is particularly important in the PNS and CNS in which RTKs mediate key events in the development and maintenance of neurons and glia through a wide range of neural processes, including survival, proliferation, differentiation, neurite outgrowth, and synaptogenesis. The mechanisms that regulate the targeting of RTKs to their subcellular destinations for appropriate signal transduction, however, are still elusive. In this review, we discuss evidence for the spatial organization of signaling machinery into distinct subcellular compartments, as well as the role for ligand specificity, receptor sorting signals, and lipid raft microdomains in RTK targeting and the resultant cellular responses in neural cells.

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“…The role of IGF1 through its receptor IGF1R signaling in the CNS and in vitro-cultured CNS cells has been well established [36][37][38][39]. In particular, IGF1R signaling is required for normal in vivo oligodendrocyte development and myelination and inhibits mature oligodendrocyte apoptosis during primary demyelination [36][37][38][39]. Thus, if IGF1R is the target of miRNA Let-7b as predicted, then the up-regulation of Let-7b in MHV-infected oligodendrocytes will down regulate the expression of IGF1R, thereby promoting apoptosis of mature oligodendrocyte and preventing myelination/remyelination and differentiation.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Cellular MicroRNA Expression in Oligodendrocytes during Acute and Persistent Coronavirus Infection

Liu¹

2015

Virol Mycol

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Genome-wide microRNA expression was profiled in oligodendrocytes during acute and persistent infection with murine coronavirus. A total of 113 microRNAs were specifically expressed in oligodendrocytes, among which 10 microRNAs were significantly upregulated while 16 microRNAs [miR-129-5p, miR-210, miR-214, miR-297, miR-297b, miR-300, miR-370, miR-466, miR-467b, miR-468, miR-669a/b, miR-672, miR-706, miR-760, and miR-801] were significantly down-regulated during infection. The biological significance of microRNA expression was further assessed for their effects on target gene expression and viral replication. Results showed that transfection of synthetic miR-214, miR-129-5p, and Let-7b specifically reduced target myelin-associated gene expression and inhibited viral replication. Importantly, there was an inverse correlation between expression of microRNAs and the level of their target genes in virusinfected cells. These results thus suggest a potential role for microRNAs in regulation of cellular gene expression in coronavirus-infected oligodendrocytes.

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Insulin-Like Growth Factor (IGF) Signaling through Type 1 IGF Receptor Plays an Important Role in Remyelination

Cited by 158 publications

References 46 publications

Suppressor of cytokine signaling 3 limits protection of leukemia inhibitory factor receptor signaling against central demyelination

Suppressor of cytokine signaling 3 limits protection of leukemia inhibitory factor receptor signaling against central demyelination

Directing traffic in neural cells: determinants of receptor tyrosine kinase localization and cellular responses

Regulation of Cellular MicroRNA Expression in Oligodendrocytes during Acute and Persistent Coronavirus Infection

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