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Pharmacologic or genetic inhibition of EphB3 receptor kinase impacts CNS pathology during progressive EAE

ABSTRACT: Pharmacologic or genetic inhibition of EphB3 receptor kinase impacts CNS pathology during progressive EAE

PROVIDER: PRJNA627395 | ENA |

REPOSITORIES: ENA

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Pharmacologic or genetic inhibition of EphB3 receptor kinase impacts CNS pathology during progressive EAE

Project description:We evaluated the role of EphB3 on the regulation of astrocyte and microglial responses and its potential as a therapeutic target during progressive EAE. We induced EAE in NOD mice that will develop a progressive form of the disease. Starting at the beginning of the progressive phase, A38 was administered and alternatively EphB3 was KD in astrocytes. Both treatments ameliorated the EAE. The transcriptional analysis of astrocytes and microglia revealed the decreased expression of genes associated to inflammation and neurodegeneration in both conditions.

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Pharmacologic inhibition of EphB3 receptor kinase ameliorates EAE

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Expression data of CNS T cells during EAE

Project description:In the absence of NR4A2 in T cells mice do not develop early acute EAE, but only a late chronic disease. We examined the mechanism by which NR4A2 can control the pathogencity of T cells in CNS autoimmune disease. To determine how NR4A2 is involved is involved in T cell pathology, we examined expression profiles of T cells during early and late diease in the presence or genetic CD4-specific absence of NR4A2. T cells infiltrating CNS tissues were isolated at peal acute EAE (D18) or during late,chronic EAE (D32). RNA expression was then analysed by genechip to determine the influence of NR4A2 in T cells on these disease stages

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Eph Receptor B3/EphrinB3 signaling impact CNS pathology during EAE

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EAE CNS Gene Expression

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Eph Receptor B3/EphrinB3 signaling impact CNS pathology during EAE

Project description:We aimed to investigate the role of EphB3 and EfnB3 on the regulation of astrocyte and microglial responses in the context of CNS inflammation, we KD Efnb3 in microglia or EphB3 in astrocytes both resulting in a comparable amelioration of EAE. The transcriptional analysis of the two cell types revealed the decreased expression of genes associated to inflammation and neurodegeneration in both KD conditions.

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Expression data of CNS T cells during EAE

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Pharmacologic inhibition of EphB3 receptor kinase ameliorates EAE

Project description:To evaluate the potential of EphB3 as a therapeutic target during CNS inflammation, we induced EAE in B6 WT mice and starting at the peak of the disease we initiated treatment with A38 administered. A38 administration ameliorated EAE, and the transcriptional analysis of the astrocytes and microglia revealed the decreased expression of genes associated to inflammation and neurodegeneration.

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Disease-associated astrocyte epigenetic memory promotes CNS pathology [RNA-Seq of p300 KD, ACLY KD and scramble NOD-EAE mice]

Project description:Gene profiling of scramble, ACLY, and p300 KD astrocytes during NOD-EAE in B6 mice.

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CSF SERPINA3 levels are increased in patients with progressive multiple sclerosis

Project description:One of the most challenging aspects in multiple sclerosis (MS) research is to understand the mechanisms leading to neurodegeneration and subsequent tissue repair. Here, we aimed to identify biomarkers associated with the progressive phases of the disease that may have neuroprotective potential. To achieve this, we performed a bioinformatic approach integrating transcriptional and proteomic profiles obtained during the course of experimental autoimmune encephalomyelitis (EAE) combined with gene expression microarray data from neuronal differentiation. Integrative analysis of omics data identified two molecules, serine (or cysteine) peptidase inhibitor, clade A, member 3N (Serpina3n) and S100 calcium binding protein A4 (S100A4), as biomarkers up-regulated in chronic progressive EAE whose expression was also induced during neuronal differentiation. Immunofluorescence studies revealed a primarily neuronal expression of Serpina3n and S100A4 during EAE as reflected by their co-localization with β-III-Tubulin in neurons from cerebellum, hippocampus and spinal cord tissues during EAE. Finally, levels of SERPINA3, the human ortholog of murine Serpina3n also known as α1-antichymotrypsin, and S100A4 were increased in cerebrospinal fluid of MS patients compared with non-inflammatory neurological controls. However, only SERPINA3 showed differences across MS clinical forms and levels were significantly elevated in patients with progressive forms of the disease, particularly in patients with primary progressive MS, compared with relapsing-remitting MS and neurological controls. Altogether, these results point to a role of SERPINA3 as biomarker associated with the progressive forms of MS that may also have neuroregenerative potential

2021-02-01 | PXD018173 | Pride

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