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Pharmacologic inhibition of EphB3 receptor kinase ameliorates EAE

ABSTRACT: Pharmacologic inhibition of EphB3 receptor kinase ameliorates EAE

PROVIDER: PRJNA627447 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11589440_1.fastq.gz	Fastqsanger.gz
	SRR11589440_2.fastq.gz	Fastqsanger.gz
	SRR11589441_1.fastq.gz	Fastqsanger.gz
	SRR11589441_2.fastq.gz	Fastqsanger.gz
	SRR11589442_1.fastq.gz	Fastqsanger.gz

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

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Project description:Genetic opticospinal EAE (OSE) and MOG-induced EAE (MOG-EAE) are two experimental autoimmune encephalomyelitis (EAE) mouse models of human multiple sclerosis. For the OSE model, double-transgenic 2D2 (TCRMOG) x IgHMOG mice were used. For MOG-EAE, wildtype C57BL/6 mice were immunized with a MOG peptide consisting of the amino acids 35-55, administered in complete Freund’s adjuvant containing 5mg / ml Mycobacterium tuberculosi. The severity of EAE was rated on the scale 0: healthy animal; 1: animal with a flaccid tail; [...]; 4: animal with both hind legs paralyzed. The case groups in the experiment were: OSE1: OSE with disease score 1; OSE4: OSE with disease score 4; MOG4: MOG-EAE injected with both MOG and adjuvant, with disease score 4. The control groups in the experiment were: OSE0: OSE with disease score 0; CFA: C57BL/6 mice injected only with adjuvant (no MOG); WT: Wildtype C57BL/6 mice. The aim of the experiment was to assess gene expression differences 1) between OSE4 and OSE0, 2) between OSE1 and OSE0, and 3) between MOG4 and CFA. For control, WT was compared to OSE0 and CFA. Subsequently, differentially expressed transcripts were compared, first, between the OSE4 vs. OSE0 and the MOG4 vs. CFA contrasts (different EAE models) and, second, between the OSE4 vs. OSE0 and the OSE1 vs. OSE0 contrasts (different EAE severity).

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