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Effects of fibroblast growth factors (FGF) on dissociated myelinating cultures

ABSTRACT: Analysis of the effects of three members of the FGF family (FGF1, FGF2 and FGF9) and bone morphogenic protein 4 (BMP4) on myelinating cultures generated from dissociated embryonic spinal cord. The results of both immediate (24 hours, T1 (24 hrs)) and long term treatments (10days, T2) give insights into the cumulative effects of sustained FGF and BMP mediated signal transduction in the pathogenesis of demyelinating diseases.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE52753 | GEO | 2015/02/18

SECONDARY ACCESSION(S): PRJNA229970

REPOSITORIES: GEO

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Effects of fibroblast growth factors (FGF) on dissociated myelinating cultures

Project description:Analysis of the effects of three members of the FGF family (FGF1, FGF2 and FGF9) and bone morphogenic protein 4 (BMP4) on myelinating cultures generated from dissociated embryonic spinal cord. The results of both immediate (24 hours, T1 (24 hrs)) and long term treatments (10days, T2) give insights into the cumulative effects of sustained FGF and BMP mediated signal transduction in the pathogenesis of demyelinating diseases. Dissociated myelinating cultures were generated from neurosphere derived astrocytes (generated from striata of P1 Sprague-Dawley rats) and spinal cord cells from E15.5 Sprague-Dawley(SD) embryos. The effect of recombinant human FGF9 and other soluble factors on these in vitro myelinating cultures was investigated by adding them to the culture media after 18 days in vitro (DIV). The effects of each factor were analysed using three independent cultures at two time points (19DIV and 28 DIV).

2015-02-18 | E-GEOD-52753 | biostudies-arrayexpress

Effects of N-terminal truncated version of FGF2 on dissociated myelinating cultures

Project description:Analysis of the effects of different FGF2 variants (human FGFs-hFGF2, wild-type protein and N-terminal truncated FGF2-F2V2) on myelinating cultures generated from dissociated embryonic spinal cord after 24 hours treatment to give insights into the effects of the N-terminal region of FGF2 on FGF signalling and its implications in demyelinating diseases.

2019-12-09 | GSE65466 | GEO

Effects of lipid-specific antibodies (sulphatide, O4) on dissociated myelinating cultures

Project description:Analysis of the effects of sulphatide specific antibody (O4, 20microg/ml) on myelinating cultures generated from dissociated embryonic rat spinal cord after 24 hours treatment to give insights into effects of lipid-specific antibodies and its implication in demyelinating diseases.

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Fibroblast growth factor 9 inhibits remyelination via an off target effect on astrocytes in multiple sclerosis

Project description:Failure of remyelination in multiple sclerosis (MS) is associated with inhibition of oligodendrocyte precursor (OPC) differentiation, but the cellular and molecular mechanisms involved remain poorly understood. We now report inflammatory demyelination in MS is associated with localized expression of fibroblast growth factor 9 (FGF9) by oligodendrocytes and to a lesser extent astrocytes, and demonstrate FGF9 inhibits myelination and remyelination in vitro. This inhibitory activity is reversible and due to an off target FGF9-dependent effect on astrocytes that disrupts in the growth factor milieu required to support myelination. We identify multiple downstream events induced by FGF9 associated with this effect including increased expression of leukaemia inhibitory growth factor (LIF) and FGF2, both of which are shown to inhibit myelination if present in excess. These studies identify FGF9-dependent signal transduction in astrocytes as a novel target for therapeutic strategies designed to enhance remyelination by endogenous OPC in MS. Gene expression profiles of rat myelinating cultures grown in the presence or absence of FGF9 (100 ng/ml) for 24h and 10 days were generated using Affymetrix GeneChipÂ® Rat Gene 1.0 ST Arrays. Each time point (T1: 24 hrs, and T2: 10 days) has Control (CTR) and Treatment (FGF) groups, with two replicates in each group. In total, 8 arrays were generated from the four groups (CTR-T1, CTR-T2, FGF-T1 and FGF-T2).

2016-02-17 | E-GEOD-44562 | biostudies-arrayexpress

Effects of lipid-specific antibodies (sulphatide, O4) on dissociated myelinating cultures

Project description:Effects of lipid-specific antibodies (sulphatide, O4) on dissociated myelinating cultures

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A PPAR?-FGF1 axis is required for adaptive adipose remodeling

Project description:We identify fibroblast growth factor 1 (FGF1) as a critical transducer in adipose tissue remodeling and link its regulation to peroxisome proliferator activated-receptor ? (PPAR?), the adipocyte master regulator and target of the thiazolidinedione (TZD) class of insulin sensitizing drugs. We show that FGF1 is highly induced in adipose tissue in response to high-fat diet (HFD) and that mice lacking FGF1 develop an aggressive diabetic phenotype coupled to aberrant adipose expansion when challenged with HFD. Mechanistically, we show that transcription of FGF1 is directly regulated by an adipocyte-selective proximal PPAR response element, and that this PPAR?-FGF1 axis is evolutionarily conserved in mammals. This work describes the first phenotype of the FGF1 knockout mouse and establishes FGF1 as a new member of the NR-FGF axis critical for maintaining metabolic homeostasis and insulin sensitization. Total RNA was obtained from epidydimal white adipose tissue (eWAT) and livers from 6 month old wild-type and FGF1-/- mice after 16 weeks on normal chow or high-fat diets.

2012-04-22 | E-GEOD-31692 | biostudies-arrayexpress

Proximity labeling by a recombinant APEX2-FGF1 fusion protein reveals interaction of FGF1 with the proteoglycans CD44 and CSPG4

Project description:Fibroblast growth factor 1 (FGF1) binds to specific FGF receptors (FGFRs) at the surface of target cells to initiate intracellular signaling. In addition, FGF1 also binds to heparan sulfate proteoglycans (HSPG), which act as important co-receptors. Even if some interactions with HSPGs have been characterized, it is not entirely clear if FGF1 could interact with additional proteoglycans at the cell surface. We have devised and tested a method to identify novel binding sites for FGF1 at the cell surface, which may also be applicable for other protein ligands. First, we constructed an APEX2-FGF1 fusion protein to perform proximal biotin labeling of proteins after binding of the fusion protein to cells. After functional validation of the construct, we used this method to identify binding sites for FGF1 on living cells. We confirmed the feasibility of our approach by easy detection of FGFR4, a well-known and specific receptor for FGF1. We then performed a screen in RPE1 cells and among the top hits were the proteoglycans CSPG4 (NG2) and CD44. We found that FGF1 binds CD44 through its heparin-binding moiety. Moreover, we found that FGF1 co-localizes with both CSPG4 and CD44 at the cell surface suggesting that these receptors act as storage molecules creating a reservoir of FGF1. Importantly, our data demonstrate that recombinant ligand-APEX2 fusion proteins can be used to identify novel receptor interactions at the cell-surface.

2018-06-06 | PXD009302 | Pride

SNAT - RNA sequencing of sorted Schwann cells as a single mixed population, enriched in myelinating Schwann cells, or enriched in not-myelinating Schwann cells

Project description:RNA sequencing of sorted mouse Schwann cells expressing YFP due to P0Cre-mediated recombination. The plotting of side scatter versus eYFP fluorescence generates 2 semi-detached eYFP+ clouds of cells, which further enables the enriched selection of myelinating Schwann cells, and of not-myelinating Schwann cells.

2021-04-22 | GSE137947 | GEO

Small RNA-Seq Reveals similar miRNA Transcriptome in Children and Young Adults with T-ALL and Indicates miR-143-3p as Novel Candidate Tumor Suppressor in This Leukemia

Project description:We aimed to identify miRNAs and pathways specifically deregulated in adolescent and young adult (AYA) T-ALL patients. Small RNA-seq showed no major differences between AYA and pediatric T-ALL, but it revealed downregulation of miR-143-3p in T-ALL patients. Prediction algorithms identified several known and putative oncogenes targeted by this miRNA, including KRAS, FGF1, and FGF9. Pathway analysis indicated signaling pathways related to cell growth and proliferation, including FGFR signaling and PI3K-AKT signaling, with the majority of genes overrepresented in these pathways being predicted targets of hsa-miR-143-3p. By luciferase reporter assays, we validated direct interactions of this miRNA with KRAS, FGF1 and FGF9. In cell proliferation assays, we showed reduction of cell growth upon miR-143-3p overexpression in two T-ALL cell lines. Our study is the first description of the miRNA transcriptome in AYA T-ALL patients and the first report on tumor suppressor potential of miR-143-3p in T-ALL. Downregulation of this miRNA in T-ALL patients might contribute to enhanced growth and viability of leukemic cells. We also discuss the potential role of miR-143-3p in FGFR signaling. Although this requires more extensive validation, it might be an interesting direction, since FGFR inhibition proved promising in preclinical studies in various cancers.

2022-09-06 | E-MTAB-11987 | biostudies-arrayexpress

A PPARγ-FGF1 axis is required for adaptive adipose remodeling

Project description:We identify fibroblast growth factor 1 (FGF1) as a critical transducer in adipose tissue remodeling and link its regulation to peroxisome proliferator activated-receptor γ (PPARγ), the adipocyte master regulator and target of the thiazolidinedione (TZD) class of insulin sensitizing drugs. We show that FGF1 is highly induced in adipose tissue in response to high-fat diet (HFD) and that mice lacking FGF1 develop an aggressive diabetic phenotype coupled to aberrant adipose expansion when challenged with HFD. Mechanistically, we show that transcription of FGF1 is directly regulated by an adipocyte-selective proximal PPAR response element, and that this PPARγ-FGF1 axis is evolutionarily conserved in mammals. This work describes the first phenotype of the FGF1 knockout mouse and establishes FGF1 as a new member of the NR-FGF axis critical for maintaining metabolic homeostasis and insulin sensitization.

2012-04-23 | GSE31692 | GEO

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