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RNA-seq analysis of bead-purified B cells of (i) 5-7-week-old Tlr779 or Tlr7WT (all Tlr9-/-) MRL/lpr mice

ABSTRACT: RNA-seq analysis of bead-purified B cells of (i) 5-7-week-old Tlr779 or Tlr7WT (all Tlr9-/-) MRL/lpr mice

PROVIDER: PRJNA1122063 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29341100.fastq.gz	Fastqsanger.gz
	SRR29341100_1.fastq.gz	Fastqsanger.gz
	SRR29341100_2.fastq.gz	Fastqsanger.gz
	SRR29341101.fastq.gz	Fastqsanger.gz
	SRR29341101_1.fastq.gz	Fastqsanger.gz

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RNA-seq analysis of bead-purified B cells of (i) 5-7-week-old Tlr779 or Tlr7WT (all Tlr9-/-) MRL/lpr mice

Project description:RNA-seq analysis of bead-purified B cells of (i) 5-7-week-old Tlr779 or Tlr7WT (all Tlr9-/-) MRL/lpr mice,stimulated or not with TLR7 agonists (CL097, invivogen) and of (ii) 5-7-week-old Tlr997 or Tlr9+/- (all Tlr7-/-) MRL/lpr mice, stimulated or not with CpG (ODN 1826, Hokkaido System Science) . The goal of this study was to evaluate if CL097 or CpG induced qualitatively different responses in Tlr7WT or Tlr779 (all Tlr9-/-) B cells and in Tlr9+/- or Tlr997 (all Tlr7-/-) B cells, respectively.

2024-12-31 | GSE269457 | GEO

RNA-seq analysis of bead-purified B cells of 5-week-old TLR9-/- MRL/lpr mice stimulated in vitro with TLR7 agonists (CL097, invivogen) or left unstimulated.

Project description:Purpose: The goal of this study was to develop a B-cell specific gene signature to catalog induced genes after short term in vitro TLR7 stimulation of TLR9-/- MRL/lpr B cells. Methods : Bead purified B cells (5M) from three 5-week-old TLR9-/- MRL/lpr mice were stimulated for 4 hours at 10M/ml with TLR7 agonist CL097 (Invivogen) at 5µg/ml or left unstimulated. RNA was isolated using the RNeasy Plus Mini Kit (QIAGEN). Samples were sequenced on an NextSeq500 (Illumina, Inc) with 2 x 75 bp paired-end reads (20 million reads per sample). Results: a B-cell specific gene signature of induced genes after short term in vitro TLR7 stimulation was cataloged.

2022-08-03 | GSE202108 | GEO

ATAC-seq analysis of aged-associated B cells (ABC) across three TLR9 genotypes (TLR9WT, TLR9-/- and non-signaling TLR9P915H/P915H) isolated from a mixed chimeric setting in the MRL/lpr murine model of systemic lupus erythematosus.

Project description:Purpose: The goal of this study was to assess if TLR9 deficiency (TLR9-/-) or TLR9 incapacity to signal through MyD88 would differentially influence the epigenetic states of ABC, in a B cell intrinsic manner. Methods : Mixed bone marrow chimeras of one-third each TLR9+/+ CD45.1/2, TLR9-/- CD45.1/1 and TLR9P915H/P915H CD45.2/2 were generated on the MRL/lpr background. From each recipient, ABC were sorted with respect to the CD45 congenic markers at [20 weeks] post chimerism. DNA was isolated using a protocol adapted from Corces et al. Samples were sequenced to obtain 20M 2x75 bp paired-end reads using an Illumina NextSeq 550 sequencer (Illumina, Inc, California, USA). Results: The majority of differences in open chromatin regions were observed between TLR9-/- and TLR9P915H ABCs. This must reflect the MyD88-independent regulatory function of TLR9 (lost in TLR9-/- and present in TLR9P915H).

2022-08-03 | GSE202103 | GEO

RNA-seq analysis of bead-purified B cells of 5-week-old TLR9-/- MRL/lpr mice stimulated in vitro with TLR7 agonists (CL097, invivogen) or left unstimulated.

Project description:RNA-seq analysis of bead-purified B cells of 5-week-old TLR9-/- MRL/lpr mice stimulated in vitro with TLR7 agonists (CL097, invivogen) or left unstimulated.

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Evaluation of microRNA levels in recipient BMMSCs of MRL/lpr mice after cell therapy (miRNA)

Project description:Mesenchymal stem cell transplantation (MSCT) has been widely used to treat a variety of human diseases. However, the detailed mechanisms underlying its success are not fully understood. Here we show that MSCT rescues recipient bone marrow mesenchymal stem cell (BMMSC) function in Fas-deficient-MRL/lpr systemic lupus erythematosus (SLE) mice via a miR-29b/Dnmt1/Notch epigenetic cascade. Using the microRNA microarray, we found that MSCT could rescue the high level of miR-29b in the recipient BMMSCs of MRL/lpr mice. In the present study, mesenchymal stem cell transplantation (MSCT) was used to treat MRL/lpr mice. One week after the treatment, normal control MSCs from C3H/HeJ mice (C3H), recipient MSCs from untreated MRL/lpr mice (LPR) and recipient MSCs from MSCT-treated MRL/lpr mice (MSC) were used for total RNA extraction and microRNA microarray for analysis of microRNA expressions.

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Project description:Up to 75% of systematic lupus erythematosus (SLE) patients experience neuropsychiatric (NP) symptoms, called neuropsychiatric SLE (NPSLE), yet the underlying mechanisms remain elusive. Microglia control synaptic pruning during early postnatal brain development. The process in NPSLE remains unclear. Here, we show that microglia-coordinated elimination of synaptic terminals participated in NPSLE in MRL/lpr mice, a lupus-prone murine model. We elucidated that lupus mice developed increased depression- and anxiety-like behaviors and persistent phagocytic microglia reactivation before overt peripheral lupus pathology. Microglial engulfment of synapses explained behavioral disorders. To elucidate the mechanism of synaptic pruning by microglia, we sequenced the gene expression in sorted microglia from both lupus (MRL/lpr) mice and the wild-type (MRL/mpj) controls.

2024-03-27 | GSE201282 | GEO

Evaluation of global methylation profile in recipient BMMSCs of MRL/lpr mice after cell therapy (MeDip)

Project description:Mesenchymal stem cell transplantation (MSCT) has been widely used to treat a variety of human diseases. However, the detailed mechanisms underlying its success are not fully understood. Here we show that MSCT rescues recipient bone marrow mesenchymal stem cell (BMMSC) function in Fas-deficient-MRL/lpr systemic lupus erythematosus (SLE) mice via rescuing their hypomethylated DNA profile. Using the methylation microarray, we found the global hypomethylation pattern in the recipient BMMSCs of MRL/lpr mice could be rescued by MSCT. In the present study, mesenchymal stem cell transplantation (MSCT) was used to treat MRL/lpr mice. One week after the treatment, normal control MSCs from C3H/HeJ mice (C3H), recipient MSCs from untreated MRL/lpr mice (LPR) and recipient MSCs from MSCT-treated MRL/lpr mice (MSC) were used for total DNA extraction and DNA methylation microarray for analysis of global genome methylation patterns.

2014-03-20 | E-GEOD-55970 | biostudies-arrayexpress

RNA-seq analysis of follicular (FO), marginal zone (MZ) and aged-associated B cells (ABC) across three TLR9 genotypes (TLR9WT, TLR9-/- and non-signaling TLR9P915H/P915H) isolated from a mixed chimeric setting in the MRL/lpr murine model of SLE

Project description:Purpose: The goal of this study was to assess if TLR9 deficiency (TLR9-/-) or TLR9 incapacity to signal through MyD88 would differentially influence the gene programs of B cell subsets, in a B cell intrinsic manner. Methods : Mixed bone marrow chimeras of one-third each TLR9+/+ CD45.1/2, TLR9-/- CD45.1/1 and TLR9P915H/P915H CD45.2/2 were generated on the MRL/lpr background. From each recipient, three B cell subsets, FO, MZ and ABC were sorted with respect to the CD45 congenic markers at [x weeks] post chimerism. RNA was isolated using the RNeasy Plus Micro Kit (QIAGEN). Samples were sequenced using NovaSeq 6000 flowcell (Illumina, Inc, California, USA) with 100 bp paired-end reads (20 million reads per sample) and aligned to the mm10 genome using the STAR aligner. Results: ABCs showed the most transcriptional differences among TLR9 genotypes. TLR9P915H and TLR9WT ABC transcriptomes were much more similar to each other than to those of TLR9-/- mice, sharing 246 of 381 DEGs, even though TLR9P915H B cells could not signal via MyD88. These included a number of genes encoding for inhibitory or anti-inflammatory pathways, suggesting that TLR9 could induce a regulatory signal independently of MyD88.

2022-08-03 | GSE181283 | GEO

miRNAs expression in kidneys tissues of MRL/lpr mice

Project description:MicroRNAs (miRNAs) have been implicated as fine-tuning regulators controlling diverse biological processes at the level of posttranscriptional repression. Dysregulation of miRNAs has been described in various disease states, including inflammatory autoimmune diseases. By using high-throughput microRNA profiling analysis, we identified a series of miRNAs dysregulated in local inflammatory lesions of human patients with autoimmune diseases, as well as their relevant mouse models such as MRL/lpr. We isolated the kidneys tissues pooled from six female MRL/lpr mice or from three control mice. Total RNA was extracted for the TaqManM-BM-. Low Density Assay v3.0

2012-12-19 | E-GEOD-37423 | biostudies-arrayexpress

Diagnosis and early detection of CNS-SLE in MRL/lpr mice using peptide microarrays (GPL14921)

Project description:We investigated whether mouse serum autoantibody binding patterns on random-sequence peptide microarrays (immunosignaturing) can be used for diagnosing and predicting the onset of lupus and its central nervous system (CNS) manifestations. Submitter states "We have no processed data to submit. We have no gpr files to submit." To identify possible predictive and diagnostic peptides of lupus and CNS-lupus, we carried out two studies and selected peptides in common across both studies. In the first study we tested 3-6 MRL/lpr, MRL/mp and C3H/HeJ mice at four months of age. For study two we tested 9-10 MRL/lpr and MRL/mp at 1.5 and 4 months of age. In both studies the mice sera were diluted 1/500 and analyzed using microarray peptides from platform GPL14921. We ran each sample in triplicate. The MRL/lpr and MRL/mp are the autoimmune strains and the C3H/HeJ is the control strain.

2014-05-08 | E-GEOD-57388 | biostudies-arrayexpress

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