Acidic FGF Expression in the Surroundings of Senile Plaques.

Kimura, Hiroshi; Tooyama, Ikuo; McGeer, Patrick L.

doi:10.1620/tjem.174.279

Cited by 15 publications

(7 citation statements)

References 86 publications

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“…In MS lesions, FGF1 was localized on astrocytes, neurons, oligodendrocytes, microglia and infiltrating T cells and B cells. Previously FGF1 was reported in neurons [ 64 ] and reactive astrocytes in Alzheimer’s disease [ 65 ]. In an animal model of chemically induced demyelination, enhanced expression of FGF1 was described during remyelination [ 66 ].…”

Section: Discussionmentioning

confidence: 99%

Transcript profiling of different types of multiple sclerosis lesions yields FGF1 as a promoter of remyelination

Mohan

Friese

Albrecht

et al. 2014

acta neuropathol commun

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Chronic demyelination is a pathological hallmark of multiple sclerosis (MS). Only a minority of MS lesions remyelinates completely. Enhancing remyelination is, therefore, a major aim of future MS therapies. Here we took a novel approach to identify factors that may inhibit or support endogenous remyelination in MS. We dissected remyelinated, demyelinated active, and demyelinated inactive white matter MS lesions, and compared transcript levels of myelination and inflammation-related genes using quantitative PCR on customized TaqMan Low Density Arrays. In remyelinated lesions, fibroblast growth factor (FGF) 1 was the most abundant of all analyzed myelination-regulating factors, showed a trend towards higher expression as compared to demyelinated lesions and was significantly higher than in control white matter. Two MS tissue blocks comprised lesions with adjacent de- and remyelinated areas and FGF1 expression was higher in the remyelinated rim compared to the demyelinated lesion core. In functional experiments, FGF1 accelerated developmental myelination in dissociated mixed cultures and promoted remyelination in slice cultures, whereas it decelerated differentiation of purified primary oligodendrocytes, suggesting that promotion of remyelination by FGF1 is based on an indirect mechanism. The analysis of human astrocyte responses to FGF1 by genome wide expression profiling showed that FGF1 induced the expression of the chemokine CXCL8 and leukemia inhibitory factor, two factors implicated in recruitment of oligodendrocytes and promotion of remyelination. Together, this study presents a transcript profiling of remyelinated MS lesions and identified FGF1 as a promoter of remyelination. Modulation of FGF family members might improve myelin repair in MS.Electronic supplementary materialThe online version of this article (doi:10.1186/s40478-014-0168-9) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Transcript profiling of different types of multiple sclerosis lesions yields FGF1 as a promoter of remyelination

Mohan

Friese

Albrecht

et al. 2014

acta neuropathol commun

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“…In a previous study of postmortem human brain, it was found that activated astrocytes have increased expression of acidic FGF (aFGF, FGF1) (7). To investigate the significance of this phenomenon, we studied the in vitro effects of aFGF on cultured human astrocytes and microglia, as well as on their surrogate U373 and THP-1 cell lines.…”

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confidence: 99%

Acidic Fibroblast Growth Factor (FGF) Potentiates Glial-mediated Neurotoxicity by Activating FGFR2 IIIb Protein

Lee

Kang

Suk

et al. 2011

Journal of Biological Chemistry

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Background: A previous study indicates that activated astrocytes increased expression of aFGF. We investigated the significance of this phenomenon. Results: We found that aFGF released by astrocytes potentiated microglial activation through FGFR2 IIIb receptors. Conclusion: We concluded that astrocytes regulate microglial activation by the aFGF-FGFR2 IIIb signaling pathway. Significance: This study suggests that astrocytes can control microglial-mediated neurodegeneration.

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“…FGF1, also known as acidic fibroblast growth factor (aFGF), involves in various biological functions including angiogenesis (Presta et al, ), wound healing (Ghielli et al, ), feeding regulation (Hanai et al, ), neurogenesis (Lee et al, ; Chen et al, ), and neuroprotection (Hashimoto et al, ). Previous studies demonstrated that FGF1 contributes to the neuroprotective activity in neuron injury or neurological disorder of animal models and human patients (Date et al, ; Cuevas et al, ; Kimura et al, ; Teng et al, ). In the patients of Alzheimer's disease, high level of FGF1 was detected in the surroundings of plaques and the number of FGF1‐expressed neurons was significantly decreased (Kimura et al, ; Thorns and Masliah, ).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies demonstrated that FGF1 contributes to the neuroprotective activity in neuron injury or neurological disorder of animal models and human patients (Date et al, ; Cuevas et al, ; Kimura et al, ; Teng et al, ). In the patients of Alzheimer's disease, high level of FGF1 was detected in the surroundings of plaques and the number of FGF1‐expressed neurons was significantly decreased (Kimura et al, ; Thorns and Masliah, ).…”

Section: Introductionmentioning

confidence: 99%

Human FGF1 promoter is active in ependymal cells and dopaminergic neurons in the brains of F1B‐GFP transgenic mice

Chen

Lin

Chiu

et al. 2014

Developmental Neurobiology

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FGF1 is involved in multiple biological functions and exhibits the importance in neuroprotective effects. Our previous studies indicated that, in human brain and retina, the FGF1B promoter controlled the expression of FGF1. However, the exact function and regulation of FGF1 in brain is still unclear. Here, we generated F1B-GFP transgenic mice that expressed the GFP reporter gene under the control of human FGF1B promoter (2540 to 131). Using the fresh brain sections of F1B-GFP transgenic mice, we found that the F1B-GFP cells expressed strong fluorescent signals in the ventricular system throughout the brain. The results of immunohistochemistry further showed that two distinct populations of F1B-GFP 1 cells existed in the brains of F1B-GFP transgenic mice. We demonstrated that one population of F1B-GFP 1 cells was ependymal cells, which distributed along the entire ventricles, and the second population of F1B-GFP 1 cells was neuronal cells that projected their long processes into multiple directions in specific areas of the brain. The double labeling of F1B-GFP 1 cells and tyrosine hydroxylase indicated that a subpopulation of F1B-GFP 1 -neuronal cells was dopaminergic neurons. Importantly, these F1B-GFP 1 /TH 1 cells were distributed in the main dopaminergic neuronal groups including hypothalamus, ventral tegmental area, and raphe nuclei. These results suggested that human FGF1B promoter was active in ependymal cells, neurons, and a portion of dopaminergic neurons. Thus, the F1B-GFP transgenic mice provide an animal model not only for studying FGF1 gene expression in vivo but also for understanding the role of FGF1 contribution in neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. V C 2014 Wiley Periodicals, Inc. Develop Neurobiol 75: 232-248, 2015

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Acidic FGF Expression in the Surroundings of Senile Plaques.

Cited by 15 publications

References 86 publications

Transcript profiling of different types of multiple sclerosis lesions yields FGF1 as a promoter of remyelination

Transcript profiling of different types of multiple sclerosis lesions yields FGF1 as a promoter of remyelination

Acidic Fibroblast Growth Factor (FGF) Potentiates Glial-mediated Neurotoxicity by Activating FGFR2 IIIb Protein

Human FGF1 promoter is active in ependymal cells and dopaminergic neurons in the brains of F1B‐GFP transgenic mice

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