Molecular characteristics of microglia in APOE-/-mice treated with APOE130-149 or control peptides after NMOSD induction
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1055467 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27316054.fastq.gz | Fastqsanger.gz | |||
| SRR27316055.fastq.gz | Fastqsanger.gz | |||
| SRR27316056.fastq.gz | Fastqsanger.gz | |||
| SRR27316057.fastq.gz | Fastqsanger.gz | |||
| SRR27316058.fastq.gz | Fastqsanger.gz |
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Project description:NMOSD is an autoimmune astrocytopathy of the central nervous system, mediated by antibodies against aquaporin-4 water channel protein (AQP4-Abs), resulting in damage of astrocytes with subsequent demyelination and axonal damage. The extracellular communication through astrocyte-derived extracellular vesicles (ADEVs) has received a growing interest in association with astrocytopathies, however, to which extent ADEVs contribute to NMOSD pathogenesis remains unclear. Here, we demonstrate a significant increase in apolipoprotein E (APOE)-rich ADEVs in AQP4-Abs-positive NMOSD patients as well as in a murine model of NMOSD.To capture further insight regarding the effects of APOE on microglial functional status, scRNA-seq was performed to identify molecular characteristics of microglia of APOE-/- mice subjected to sham or NMOSD induction and treated with APOE130-149 or control peptides. We demonstrated that APOE130-149 treatment has a substantial effect on microglial transcriptomes and biological features, suppressing molecules associated with microglia activation and pro-inflammatory functions.
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Project description:The multi-ligand Receptor for AGE (RAGE) contributes to atherosclerosis in apolipoprotein (ApoE) null mice in both the non-diabetic and diabetic states. Previous studies using soluble RAGE, the extracellular ligand-binding domain of RAGE, or homozygous RAGE null mice showed that blockade or deletion of RAGE resulted in marked reduction in atherosclerotic lesion area and complexity compared to control animals. In parallel, significant down-regulation of inflammatory mediators and matrix metalloproteinases was evident in ApoE null mice aortas devoid of RAGE compared to those of ApoE null RAGE-expressing mice. Although these findings suggested that RAGE triggered pro-atherogenic mechanisms via regulation of inflammatory gene expression, these studies did not reveal the broader pathways by which RAGE contributed to atherosclerosis in ApoE null mice. Therefore, we performed Affymetrix gene expression arrays on aortas of non-diabetic and diabetic ApoE null mice expressing RAGE or devoid of RAGE at nine weeks of age, as this reflected a time point at which frank atherosclerotic lesions were not yet present, but, that we would be able to identify the genes likely involved in diabetes- and RAGE-dependent atherogenesis. The comparisons were as follows: 1. diabetic ApoE null relative to non-diabetic ApoE null; 2. non-diabetic ApoE null / RAGE null relative to non-diabetic ApoE null; 3. diabetic ApoE null / RAGE null relative to non-diabetic ApoE null / RAGE null; and 4. diabetic ApoE null / RAGE null relative to diabetic ApoE null aorta. Our data reveal that there is very little overlap of the genes which are differentially expressed both in the onset of diabetes in ApoE null mice, and in the effect of RAGE deletion in diabetic ApoE null mice. We next performed a Pathway-Express analysis to determine the pathways that were most associated with the onset of diabetes in ApoE null mice and the effect of RAGE gene deletion in diabetic ApoE null mice. Rigorous statistical analysis was undertaken and revealed that the transforming growth factor-beta pathway (tgf-beta) and focal adhesion pathways might be expected to play a significant role in both the mechanism by which diabetes facilitates the formation of atherosclerotic plaques in ApoE null mice, and the mechanism by which deletion of RAGE ameliorates this effect. We focused on three genes of the tgf-betafamily which were found to be up-regulated in diabetic vs. non-diabetic ApoE null aorta, and which were reduced by deletion of RAGE. These included: thrombospondin1 (Thbs1), transforming growth factor-beta (tgf-beta) and rho-associated kinase (ROCK1). Real-time quantitative polymerase chain reaction and Western blotting experiments were performed, as well as ROCK1 activity assays in mouse aorta, and validated the findings of the Affymetrix gene array. Further, confocal microscopy revealed that a principal cell type in the ApoE null aorta expressing these factors was the vascular smooth muscle cell. Our data suggest the novel finding that the observed reduction of accelerated atherosclerosis in diabetic ApoE null / RAGE null vs. diabetic ApoE null mice occurs, all or in part, through the ROCK1 branch of the TGF-betapathway. We have inferred a detailed mechanism for this process. Taken together, these data suggest that suppression of ROCK1 activity in the atherosclerosis-vulnerable vessel wall, especially in diabetes, but in non-diabetes as well, may underlie the beneficial effects of RAGE antagonism and genetic deletion in murine models. These findings highlight logical and novel targets for therapeutic intervention in cardiovascular disease and diabetes. 1. diabetic ApoE null relative to non-diabetic ApoE null; 2. non-diabetic ApoE null / RAGE null relative to non-diabetic ApoE null; 3. diabetic ApoE null / RAGE null relative to non-diabetic ApoE null / RAGE null; and 4. diabetic ApoE null / RAGE null relative to diabetic ApoE null aorta. There were 4 mice in each group initially. However there are only 3 non-diabetic ApoE null / RAGE null mice in the final experimental sample in group 3 due to a failure to generate cRNA from that sample. All samples were normalized to remove chip-dependent regularities using the RMA method. Chips and controls at each combination of genotype and disease sate were normalized together. The statistical significance of differential expression was calculated using the empirical Bayesian LIMMA (LInear Model for MicroArrays) method A cut-off B>0 was used for the statistical significance of gene expression.
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Project description:Morchella steppicola PhC 149 Transcriptome - Morpa-RNA1
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Project description:Results of knocking-down AREG expression in SUM-149 cells by lenitviral infection of shRNA vectors and measuring gene expression provides information as to what genes are regulated by AERG in inflammatory breast cancer cells.
2010-12-15 | GSE26079 | GEO
Project description:Flavobacterium glycines Gm-149 genome sequencing
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Project description:Results of knocking-down AREG expression in SUM-149 cells by lenitviral infection of shRNA vectors and measuring gene expression provides information as to what genes are regulated by AERG in inflammatory breast cancer cells. SUM-149 cells were infected with a single AREG shRNA virus (sh4) or three AREG shRNA viruses (shPld) and the non-silencing vector (shNS). Total RNA was collected and genome-wide analysis of expression was performed on RNA from each cell line.
2010-12-15 | E-GEOD-26079 | biostudies-arrayexpress