Fibroblast growth factor 2 (FGF2) and FGF receptor expression in an experimental demyelinating disease with extensive remyelination

Messersmith, Donna J.; Murtie, Joshua; Le, Tai; Frost, Emma E.; Armstrong, Regina C.

doi:10.1002/1097-4547(20001015)62:2<241::aid-jnr9>3.0.co;2-d

Cited by 147 publications

(111 citation statements)

References 78 publications

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“…A mouse monoclonal IgG 1 antibody directed against phosphorylated and nonphosphorylated high molecular weight neurofilaments (NF-H; 1:1000; Sternberger Monoclonals) was used to detect axons. The mouse monoclonal IgG 2B antibody CC1 (1:10; Oncogene, Uniondale, NY) was used as a marker for mature oligodendrocytes (Messersmith et al, 2000). The rabbit polyclonal NG2 antibody (1:100) was used as a marker for oligodendrocyte progenitors (Nishiyama et al, 1996).…”

Section: Methodsmentioning

confidence: 99%

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

et al. 2003

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We examined the role of IGF signaling in the remyelination process by disrupting the gene encoding the type 1 IGF receptor (IGF1R) specifically in the mouse brain by Cre-mediated recombination and then exposing these mutants and normal siblings to cuprizone. This neurotoxicant induces a demyelinating lesion in the corpus callosum that is reversible on termination of the insult. Acute demyelination and oligodendrocyte depletion were the same in mutants and controls, but the mutants did not remyelinate adequately. We observed that oligodendrocyte progenitors did not accumulate, proliferate, or survive within the mutant mice, compared with wild type, indicating that signaling through the IGF1R plays a critical role in remyelination via effects on oligodendrocyte progenitors.

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Section: Methodsmentioning

confidence: 99%

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

et al. 2003

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“…Indeed, astroglia upregulates the expression of an enormous array of GFs (Fig. 1a, b), including nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF; [47]), neurotrophin-3 (NT-3; [48]), CNTF (see above), vascular endothelial growth factor (VEGF; [49]), epidermal growth factor (EGF; [50]), basic fibroblast growth factor (bFGF; [51,52]), insulin growth factor 1 (IGF1; [53]) and glial cell-line derived neurotropic factor (GDNF; [54]). GFs play a key role in pathological conditions, when they trophically support damaged neurons, oligodendrocytes, and, in some instances, activated progenitor cells (see Section 3.2).…”

Section: Cytokines and Growth Factorsmentioning

confidence: 99%

Astrocytes in the damaged brain: Molecular and cellular insights into their reactive response and healing potential

Buffo

Rolando

Ceruti

2010

Biochemical Pharmacology

288

260

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 2 Running title: Beneficial and detrimental outcomes of astrogliosis after central nervous system injury. Abbreviations:Ado, adenosine; AMPA, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate; AP1, activator protein1; AQP, acquaporin; BBB, blood-brain barrier; BDNF, brain-derived growth factor; bFGF, basic fibroblast growth factor; bHLH, basic helix loop helix; BMP, bone morphogenetic protein; CNS, central nervous system; CNTF, ciliary neurotrophic factor;COX-2, cyclooxigenase-2; CREB, cAMP response element binding; CSPGs, chondroitinsulphate proteoglycans; ERK, extracellular signal-regulated kinase; EGF, epidermal growth factor; Eph4A, ephrin 4A; Epo, erythropoietin; ET1, Endothelin 1; ET-R, endothelin receptor; GABA, gamma-aminobutyric acid; GDNF, glial cell-line derived neurotropic factor; GF, growth factor; GFAP, glial fibrillary acidic protein; GLAST, glutamate aspartate transporter; GLT1, glutamate transporter 1; GS, glutamine synthase; IFN , interferon-beta; IFNγ, interferon gamma; IGF1, insulin growth factor1; IL1β, interleukin 1 beta; IL2, interleukin 2; IL6, interleukin 6; IL10, interleukin 10; JAK, Janus protein tyrosine kinases; Lcn2, Lipocalin 2; MAPK, mitogen-activated protein kinase; MMP, matrix metalloprotease; mTOR, mammalian target of rapamycin; NFAT, nuclear factor of activated T cell; NFkB, nuclear factor kappa B; NGF, nerve growth factor; NT3, neurotrophin 3; p38MAPK, p38 mitogen-activated protein kinase; PTEN, phosphatase and tensin homolog; SOCS, suppressor of cytokine signaling; SOD, superoxide dismutase; STAT, signal transducers and activators of transcription; TGFα, transforming growth factor alpha;TGFβ, transforming growth factor beta; TNFα, tumor necrosis factor alpha; VCAM1, vascular cell adhesion molecule-1; VEGF, vascular endothelial growth factor. Page 4 of 63A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 4...

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“…Areas of acute and chronic demyelination have increased expression of FGF2 ligand and FGF receptors [11,26,36,37]. In contrast with predictions from in vitro studies, OP proliferation in demyelinated lesions was not impaired in FGF2-null mice, indicating that the potential for FGF2 to act as an OP mitogen may not be a significant role of endogenous FGF2 in vivo during demyelination [37].…”

Section: Stimulating Proliferation To Counter Op Depletion In Chronicmentioning

confidence: 99%

Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS

Armstrong

2007

Future Neurol.

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Remyelination facilitates recovery of saltatory conduction along demyelinated axons and may help prevent axon damage in patients with demyelinating diseases, such as multiple sclerosis. The extent of remyelination in multiple sclerosis lesions varies dramatically, indicating a capacity for repair that is not fulfilled in lesions with poor remyelination. In experimental models of demyelinating disease, remyelination is limited by chronic disease that depletes the oligodendrocyte progenitor (OP) population, inhibits OP differentiation into remyelinating oligodendrocytes and/or perturbs cell survival in the lesion environment. Manipulating the activity of growth factor signaling pathways significantly improves the ability of endogenous OP cells to accomplish extensive remyelination. Specifically, growth factors have been identified that can regulate OP proliferation, differentiation and survival in demyelinated lesions. Therefore, growth factors may be key signals for strategies to improve conditions with poor remyelination. Keywords cuprizone; demyelinating disease; FGF; multiple sclerosis; myelin; oligodendrocyte; PDGF; progenitors; remyelination Transition to in vivo analysis during remyelinationAnalysis of growth factors to promote repair in demyelinating diseases has undergone an important transition to in vivo studies and in doing so has revealed much more than the expected results. Characterization of the bipotential oligodendrocyte-type 2 astrocyte or oligodendrocyte progenitor (OP) cell, and the regulation of cell fate by serum components [1] opened the door for in vitro analysis of growth factor responses in the oligodendrocyte lineage. Numerous subsequent in vitro studies identified specific growth factors capable of regulating differentiation, proliferation, migration and survival at specific stages within this lineage. In vitro studies continue to offer distinct advantages for isolating molecular and cellular mechanisms of action and for characterizing the potential of defined growth factors to induce a specific cellular response. In this context, several cytokines and chemokines have been identified as having direct effects on oligodendrocyte lineage cells that are similar to growth factor actions and so they will be discussed together under the rubric of growth factors. This review will focus on recent in vivo remyelination studies designed to test potential growth factor responses identified in vitro. These in vivo studies demonstrate important effects of growth factors in the context of demyelinating disease models in rodents. However, not all growth factor analyses have resulted in the predicted responses. Importantly, several studies have demonstrated a remarkable capacity of endogenous cells to repair the adult CNS, even following chronic demyelination, using modulation of growth factor signaling to better support oligodendrocyte replacement and myelin formation.

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Fibroblast growth factor 2 (FGF2) and FGF receptor expression in an experimental demyelinating disease with extensive remyelination

Cited by 147 publications

References 78 publications

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

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

Astrocytes in the damaged brain: Molecular and cellular insights into their reactive response and healing potential

Growth factor regulation of remyelination: behind the growing interest in endogenous cell repair of the CNS

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