Fibroblast Growth Factors and Their Receptors in Oligodendrocyte Development: Implications for Demyelination and Remyelination

Bansal, Rashmi; Miyake, Hideaki; Nakamura, Ichiro; Eto, Hiroshi; Gotoh, Akinobu; Fujisawa, Masato; Okada, Hiroshi; Arakawa, Soichi; Kamidono, Sadao; Hara, Isao

doi:10.1159/000064944

Cited by 79 publications

(77 citation statements)

References 86 publications

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“…Multiple lines of evidence predict an important role for Fgfr2 in OL differentiation and myelin membrane formation (Bansal, 2002;Fortin et al, 2005). Thus, the absence of defects of OL development and myelination in Fgfr2 conditional knock-out mice was unexpected.…”

Section: Discussionmentioning

confidence: 99%

“…This signaling is mediated by four FGF receptors (Fgfr1-Fgfr4) and a subset of ligand FGFs expressed in the brain from a family of 22 members (OrrUrtreger et al, 1993;Miyake et al, 1996;Ford-Perriss et al, 2001;Bansal et al, 2003). These FGF ligand-receptor complexes play diverse roles in the regulation of proliferation, migration, differentiation, and survival of both neurons and glia (Vaccarino et al, 1999;Ford-Perriss et al, 2001), including oligodendrocytes (OLs), the myelin-forming cells of the CNS (for review, see Bansal, 2002;Fortin et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Mice with Conditional Inactivation of Fibroblast Growth Factor Receptor-2 Signaling in Oligodendrocytes Have Normal Myelin But Display Dramatic Hyperactivity when Combined with Cnp1 Inactivation

Kaga¹,

Shoemaker²,

Furusho³

et al. 2006

J. Neurosci.

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Fibroblast growth factor receptors (Fgfr) comprise a widely expressed family of developmental regulators implicated in oligodendrocyte (OL) maturation of the CNS. Fgfr2 is expressed by OLs in myelinated fiber tracks. In vitro, Fgfr2 is highly upregulated during OL terminal differentiation, and its activation leads to enhanced growth of OL processes and the formation of myelin-like membranes. To investigate the in vivo function of Fgfr2 signaling by myelinating glial cells, we inactivated the floxed Fgfr2 gene in mice that coexpress Cre recombinase (cre) as a knock-in gene into the OL-specific 2Ј,3Ј-cyclic nucleotide phosphodiesterase (Cnp1) locus. Surprisingly, no obvious defects were detected in brain development of these conditional mutants, including the number of OLs, the onset and extent of myelination, the ultrastructure of myelin, and the expression level of myelin proteins. However, unexpectedly, a subset of these conditional Fgfr2 knock-out mice that are homozygous for cre and therefore are also Cnp1 null, displayed a dramatic hyperactive behavior starting at ϳ2 weeks of age. This hyperactivity was abolished by treatment with dopamine receptor antagonists or catecholamine biosynthesis inhibitors, suggesting that the symptoms involve a dysregulation of the dopaminergic system. Although the molecular mechanisms are presently unknown, this novel mouse model of hyperactivity demonstrates the potential involvement of OLs in neuropsychiatric disorders, as well as the nonpredictable role of genetic interactions in the behavioral phenotype of mice.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mice with Conditional Inactivation of Fibroblast Growth Factor Receptor-2 Signaling in Oligodendrocytes Have Normal Myelin But Display Dramatic Hyperactivity when Combined with Cnp1 Inactivation

Kaga¹,

Shoemaker²,

Furusho³

et al. 2006

J. Neurosci.

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“…For example, galactolipids are influential in oligodendrocyte development and maturation (Bansal and Pfeiffer, 1989;Marcus et al, 2000). Similarly, fibroblast growth factor-2 potently inhibits oligodendrocyte maturation by stimulating proliferation and preventing terminal differentiation (Bansal, 2002). Whether there is any relationship between ErbB4 activity and the effects on oligodendrocyte maturation by these factors is unknown.…”

Section: Absence Of Erbb4 Modified Oligodendrocyte Lineage Maturationmentioning

confidence: 99%

The ErbB4 Neuregulin Receptor Mediates Suppression of Oligodendrocyte Maturation

Sussman

Vartanian

Miller

2005

Journal of Neuroscience

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Neuregulin is required for proper oligodendrocyte development, but which receptors are involved and whether neuregulin promotes or inhibits maturation remain controversial. To assess the roles of the neuregulin receptor ErbB4 in oligodendrocyte development, we examined oligodendrocyte initiation and maturation in cultures derived from erbB4 knock-out mice and rat spinal cord in the presence of neutralizing erbB4 antibodies. No differences in the development of O4 ϩ oligodendrocytes were detected in the presence or absence of erbB4 signaling. All four epidermal growth factor receptor family members were detected in the ventral neural tube at approximately the time of initial oligodendrocyte development, consistent with redundancy in neuregulin receptor signaling at the onset of oligodendrocyte development. In contrast, greater numbers of differentiated (monoclonal antibody O1 ϩ ) oligodendrocytes developed in neural tube explants from erbB4 ؊/؊ mice than either erbB4 ؉/؉ or erbB4 ؉/؊ littermates as well as in cultures treated with anti-erbB4. These data indicate that ErbB4 is not required for oligodendrocyte development and, in fact, inhibits oligodendrocyte lineage maturation. Together with previous studies, these data suggest a model in which early oligodendrocyte lineage development is regulated by promiscuous neuregulin receptor signaling, but subsequent lineage progression occurs through a balance of receptor-specific promotion or inhibition of maturation.

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“…The HS side chains of these PGs consist of a glucosamine-uronic acid backbone, variably and regionally modified by N-acetylations, N-sulfations, and O-sulfations, providing numerous binding sites for polybasic molecules, especially growth factors (for recent reviews, see Refs. [1][2][3][4][5]. The cell surface HSPG glypican-1 (Gpc-1) is specifically up-regulated in glioma vessels, leading to enhanced tumor growth (6).…”

mentioning

confidence: 99%

Involvement of Glycosylphosphatidylinositol-linked Ceruloplasmin in the Copper/Zinc-Nitric Oxide-dependent Degradation of Glypican-1 Heparan Sulfate in Rat C6 Glioma Cells

Mani

Cheng

Havsmark

et al. 2004

Journal of Biological Chemistry

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Fibroblast Growth Factors and Their Receptors in Oligodendrocyte Development: Implications for Demyelination and Remyelination

Cited by 79 publications

References 86 publications

Mice with Conditional Inactivation of Fibroblast Growth Factor Receptor-2 Signaling in Oligodendrocytes Have Normal Myelin But Display Dramatic Hyperactivity when Combined with Cnp1 Inactivation

Mice with Conditional Inactivation of Fibroblast Growth Factor Receptor-2 Signaling in Oligodendrocytes Have Normal Myelin But Display Dramatic Hyperactivity when Combined with Cnp1 Inactivation

The ErbB4 Neuregulin Receptor Mediates Suppression of Oligodendrocyte Maturation

Involvement of Glycosylphosphatidylinositol-linked Ceruloplasmin in the Copper/Zinc-Nitric Oxide-dependent Degradation of Glypican-1 Heparan Sulfate in Rat C6 Glioma Cells

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