Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell RNA sequencing of femur bone marrow cells from the NZBWF1 systemic lupus erythematosus mouse model and its progenitors.

ABSTRACT: Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by failure of self-tolerance mechanisms and the resultant production of autoreactive antibodies. The NZBWF1 mouse spontaneously develops a lupus-like syndrome and is used as model of SLE. The NZBWF1 model represents the F1 generation of a cross between New Zealand Black (NZB) and New Zealand White (NZW) mice. In this study we investigated the model and its progenitors (NZB, NZW) gene expression with single cell RNA sequencing on cells isolated from bone marrow and processed with the 10X Chromium.

ORGANISM(S): Mus musculus

PROVIDER: GSE174728 | GEO | 2021/05/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Diosmetin blocks type Ⅰ interferon signaling by metabolic control of phosphatidylethanolamine [dataset 2]

Project description:Type I interferon (IFN-I) is essential in the development of Systemic Lupus Erythematosus (SLE) and many other autoimmune diseases. To explore the metabolic regulations of IFN-I signaling pathway, we conducted a high through-put screening of a small molecule library and identified diosmetin as a potent compound for blocking IFN-I signaling. Diosmetin can ameliorate lupus-like autoimmune phenotypes in IFNα-accelerated NZB/NZW F1 lupus model and pristane-induced murine lupus model. Of note, diosmetin can block over-activated IFN-I signaling pathway in PBMCs from lupus patients by reducing the expression of CYP1B1. Our findings reveal a novel lipid metabolic regulation of IFN-I signaling and a potent alternative therapeutic target for autoimmune diseases with overactivated IFN-I signaling pathway.

2023-07-06 | GSE236320 | GEO

Diosmetin blocks type Ⅰ interferon 1 signaling by metabolic control of phosphatidylethanolamine [dataset 1]

2023-07-06 | GSE236319 | GEO

Human and mouse lupus nephritis cross-species transcriptional analysis

Project description:This SuperSeries is composed of the following subset Series: GSE32583: Expression data from lupus NZB/W, NZM2410, NZW/BXSB mouse kidneys prenephritic and nephritic. GSE32591: Expression data from human with lupus nephritis (LN) Refer to individual Series

2012-08-01 | E-GEOD-32592 | biostudies-arrayexpress

Identification of common lupus-disease related microRNA expression pattern in three different murine models of lupus

Project description:In this study, miRNA expression in splenic lymphocytes from three genetically disparate lupus-prone mouse models (MRL-lpr, B6-lpr and NZB/WF1) were profiled. 49 miRNAs were found to be differentially expressed in MRL-lpr mice compared to MRL mice; and 24 miRNAs were differentially expressed in B6-lpr mice compared to B6 mice. Among these dysregulated miRNAs, we noted that 15 miRNAs were common to both lpr strains. Interestingly, microarray analysis of NZB/W and NZW at 3 months of age, an age when overt lupus disease is not evident in NZB/W mice, revealed that only one miRNA, miR-148a was significantly upregulated in NZB/W mice. The aim of this porject is to determine the common miRNA expression changes in splenocytes from different strains of murine lupus models. The splenocytes were prepared from genetically lupus-prone female mice including MRL/MpJ-Faslpr/J (MRL-lpr), NZBWF1/J (NZB/W), B6.MRL-Faslpr/J (B6-lpr) and their control mice MRL/MpJ (MRL), NZW/LacJ (NZW) and C57BL/6J (B6) mice (The Jackson laboratory, ME). Total RNAs, containing miRNAs were isolated from whole splenocytes using mirVana miRNA isolation kits (Ambion) following manufactory’s instructions and sent to LC Sciences (http://www.lcsciences.com/) for the microarray assay. The mouse miRNA array chips (Chip ID miRMouse 12.0 version), which included 617 unique, mature, mouse miRNA, based on the Sanger miRBase Release 12.0, were used in the assay.

2011-12-17 | E-GEOD-22359 | biostudies-arrayexpress

Gene expression analysis in T cells from spleens of mice that provide a model for systemic lupus erythematosus

Project description:This laboratory focuses on the interactions of murine CD4+CD25+ regulatory T cells (Tregs) with CD4+CD25- T cells, both from a fundamental biological point of view, and in the context of a murine model of lupus. This study characterized the surface glycans expressed by CD25 and CD25- CD4 T cells selected from lupus-prone (systemic lupus erythematosus or SLE) mouse strains MRL/Mp and NZB/W F1 and two control strains, CBA/Ca (haplotype-matched with the MRL/Mp; H-2k) and BALB/c. A transcriptomic survey of freshly isolated and bead-activated CD25 and CD25- CD4 T cells selected from mouse spleens was conducted using these four strains. Three replicate samples of each condition were hybridized to the GLYCOv2 array, for a total of 48 samples.

2011-03-02 | E-GEOD-27591 | biostudies-arrayexpress

Kidney gene expression profiles from a lupus nephritis mouse model: NZB X NZW F1 (BWF1) mice treated with IFN-alpha with adenovirus delivery.

Project description:We characterized the longitudinal gene expression profiles of kidneys from a lupus model nephtiris: NZB X NZW F1 (BWF1) mice treated with IFN-alpha using adenovirus delivery. Genes from biological processes such as IFN response, complement, Fc gamma receptors, immune recruitment, innate immune pattern recognition, antibody response and fibrosis,were upregulated in diseased kidneys.

2016-09-06 | GSE86423 | GEO

Identification of common lupus-disease related microRNA expression pattern in three different murine models of lupus

2011-12-17 | GSE22359 | GEO

Transcriptomes of splenocytes from 16-week-old lupus-prone female NZB/NZW F1 mice and non-lupus-prone male NZB/NZW F1 and female BALB/c mice

Project description:Transcriptomic analysis of gene expression of splenocytes from 16-week-old female NZB/NZW F1 (BWF1) mice, which are prone to lupus, and comparison to gene expression of splenocytes from male BWF1 and female BALB/c mice, which are not prone to lupus. Results provide insight into the differences in immunological activities that make female BWF1 mice more susceptible to lupus.

2021-04-01 | GSE167273 | GEO

Transcriptomic data for splenic neutrophils isolated from female NZBWF1/J lupus mice

Project description:Recent literature has shown that neutrophils exert significant influence on the course of disease progression in lupus, but there is currently controversy in the lupus field regarding a) whether neutrophils are predominantly protective or deleterious toward the propagation of auto-reactivity, b) the specific mechanism of neutrophil influence on adaptive immune dysregulation, and c) identity and origin of functionally abnormal neutrophil subsets in lupus. Here we used RNA sequencing of splenic neutrophils isolated from a murine lupus model (NZB/W) to characterize changes in the transcriptional program of neutrophils over the course of lupus progression. We find that the transcription of immunologically relevant genes change over the course of disease, and that lupus neutrophils early in disease show enrichment for transcripts associated with neutrophil precursors. These data provide the first detailed profile of the splenic neutrophil transcriptional program changes during the progression of lupus.

2017-05-10 | GSE97439 | GEO

p55 and p75 tumor necrosis factor receptor double KO and systemic lupus erythematosis

Project description:Gene expresion comperison of p55/p75 double knock and it control B57B6 identified a number of inflammatory genes and cytokines genes play important roles in this study. TNFa has both pro-inflammatory and immunoregulatory functions. Whereas a protective role for TNF administration in SLE-prone (NZB x NZW)F1 mice has been established, it remains uncertain whether this effect segregates at the individual TNF receptors (TNFR). We generated SLE-prone New Zealand Mixed 2328 mice genetically deficient in TNF receptor 1, in TNF receptor 2, or in both receptors. Doubly-deficient mice developed accelerated pathological and clinical nephritis with elevated levels of circulating IgG anti-dsDNA autoantibodies and increased numbers of CD4+ T lymphocytes, especially activated memory (CD44highCD62Llow) CD4+ T cells. We show that these cells expressed a Th17 gene profile, were positive for IL-17 intracellular staining by FACS, and produced exogenous IL-17 in culture. In contrast, immunological, pathological, and clinical profiles of mice deficient in either TNF receptor alone did not differ from those in each other or from those in wild-type controls. Thus, total ablation of TNFa-mediated signaling was highly deleterious to the host in the NZM 2328 SLE model. These observations may have profound ramifications for the use of TNF- and TNF receptor-antagonists in human SLE and related autoimmune disorders, as well as demonstrate, for the first time, the association of the Th17 pathway with an animal model of SLE.

2009-12-06 | GSE13855 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data