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Transcriptome analysis of human astrocytes upon FGF1 stimulation

ABSTRACT: In a previous study performed in our laboratory, the level of FGF1 RNA was found to be increased in remyelinated multiple sclerosis lesions compared to control brain (unpublished observation). Astrocytes play a key role in multiple sclerosis lesion formation. To shed light on potential FGF1-mediated functions in multiple sclerosis, the impact of FGF1 on astrocytes was investigated.

ORGANISM(S): Homo sapiens

SUBMITTER: Anita Friese

PROVIDER: E-MTAB-2485 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Mohan Hema H Friese Anita A Albrecht Stefanie S Krumbholz Markus M Elliott Christina L CL Arthur Ariel A Menon Ramesh R Farina Cinthia C Junker Andreas A Stadelmann Christine C Barnett Susan C SC Huitinga Inge I Wekerle Hartmut H Hohlfeld Reinhard R Lassmann Hans H Kuhlmann Tanja T Linington Chris C Meinl Edgar E

Acta neuropathologica communications 20141211

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 q ...[more]

PMID: 25589163

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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

Rapid reprogramming of primary human astrocytes into potent tumor initiating cells with defined genetic factors

Project description:Cancer stem cells play key roles in human malignancies. However, their cellular and molecular origins are still poorly understood. Here we report the successful generation of cancer stem cells from primary human astrocytes by use of defined genetic factors. Combined transduction of four factors âmyc, Oct-4, p53DD, and rasâ induced efficient transformation of primary human astrocytes into malignant cells with powerful tumor-initiating capabilities. Transplantation of 100 of the cells into nude mice is sufficient for tumor formation. The cells also showed unlimited self-renewal ability with robust telomerase activities. In addition, they expressed typical glioma stem cell markers such as CD133, CD15, and CD90. Moreover, transformed cells could form spheres in culture and differentiate into neuron-astrocyte-, and oligodendrocyte-like cells. They also displayed significant resistance to temozolomide. These induced cancer stem cells (iCSCs) should be useful for both tumor biology studies and therapeutics development. This record contains data from microarray analysis of normal human astrocytes, two transduced cell lines (OCT4+3G and OCT4+6G), a patient-derived glioma stem cell line (ALPS1459) and a glioblastoma cell line (U87MG).

2016-11-07 | E-MTAB-4771 | biostudies-arrayexpress

Expression data from SHP specific siRNA or nonspecefic siRNA transfected rat astrocytes

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2016-01-21 | E-GEOD-76704 | biostudies-arrayexpress

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2024-08-13 | E-MTAB-14327 | biostudies-arrayexpress

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

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

Direct reprogramming of human astrocytes into neural stem cells and neurons

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2013-12-01 | E-GEOD-36145 | biostudies-arrayexpress

Perturbations of the proteome in primary astrocytes from the hSOD1(G93A) ALS mouse model

Project description:Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease whose pathophysiology is largely unknown. Despite motor neuron death is recognized as the key event in ALS, astrocytes dysfunctionalities and neuroinflammation were demonstrated to accompany and probably even drive motor neuron loss. Nevertheless, the mechanisms priming astrocyte failure and hyperactivation are still obscure. In this work, altered pathways in ALS astrocytes were unveiled by investigating the proteomic profile of primary spinal-cord astrocytes derived from transgenic ALS mouse model overexpressing the human (h)SOD1(G93A) protein, in comparison with the transgenic counterpart expressing hSOD1(WT) protein. In this research, we showed that hSOD1(G93A) astrocytes present a profound alterations in the expression of proteins involved in proteostasis and glutathione metabolism.

2022-02-17 | PXD026576 | Pride

Mouse primary astrocytes: LCN2 protein treated vs. control

Project description:Transcriptional profiling of mouse primary astrocytes comparing control untreated astrocytes with astrocytes treated with recombinant LCN2 protein (10 micro gram/ml). Goal was to determine the effects of LCN2 treatment on global gene expression in astrocytes. A secreted protein lipocalin-2 (LCN2) has been implicated in diverse cellular processes including cell morphology and migration. We have previously demonstrated that lcn2 mediates reactive astrocytosis. In order to further understand the role of lcn2 in the CNS, astrocyte transcriptome was analyzed following LCN2 treatment. Chemokines were the major group of genes upregulated by LCN2. Two-condition experiment, control untreated astrocytes vs. LCN2 protein treated astrocytes. Biological replicates: 1 control replicates, 1 treated replicates.

2012-06-29 | E-GEOD-15667 | biostudies-arrayexpress

Transcription profiling of neurons or astrocytes treated with grape seed extract

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2009-04-18 | E-GEOD-15285 | biostudies-arrayexpress

A SUMOylated C-terminus fragment of glutamate transporter EAAT2 linked to inherited ALS mediates motor axon impairment

Project description:Downregulation of expression and activity levels of the astroglial glutamate transporter EAAT2 is thought to be implicated in motor neuron excitotoxicity in amyotrophic lateral sclerosis (ALS). We previously reported that EAAT2 is cleaved by caspase-3 at the cytosolic C-terminus domain, impairing the transport activity and generating a proteolytic fragment found to be SUMO1 conjugated (CTE-SUMO1). We show here that this fragment accumulates in the nucleus of spinal cord astrocytes in vivo throughout the disease stages of the SOD1-G93A mouse model of ALS. In vitro expression in spinal cord astrocytes of the C-terminus peptide of EAAT2 (CTE), which was artificially fused to SUMO1 (CTE-SUMO1fus) to mimic the endogenous SUMOylation reaction, recapitulates the nuclear accumulation of the fragment seen in vivo and causes caspase-3 activation and axonal growth impairment in motor neuron-derived NSC-34 cells and primary motor neurons co-cultured with CTE-SUMO1fus-expressing spinal cord astrocytes. This indicates that CTE-SUMO1fus could trigger non-cell autonomous mechanisms of neurodegeneration. Prolonged nuclear accumulation of CTE-SUMO1fus in astrocytes leads to their degeneration, although the time frame of the cell-autonomous toxicity is longer than the one for the indirect toxic effect on motor neurons. As more evidence on the implication of SUMO substrates in neurodegenerative diseases emerges, our observations strongly suggest that the nuclear accumulation in spinal cord astrocytes of a SUMOylated proteolytic fragment of the astroglial glutamate transporter EAAT2 could take part to the pathogenesis of ALS and suggest a novel, unconventional role for EAAT2 in motor neuron degeneration in ALS. Comparison is made between the toxic fragment (SUMO) and the same fragment without lysines that can be sumo-ylated (CTE). Four replicates have been performed for each sample group.

2011-07-19 | E-GEOD-26070 | biostudies-arrayexpress

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