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Retinoic acid exerts disease stage-dependent effects on pristane-induced lupus

ABSTRACT: Retinoic acid exerts disease stage-dependent effects on pristane-induced lupus

PROVIDER: PRJNA588259 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10417126_1.fastq.gz	Fastqsanger.gz
	SRR10417126_2.fastq.gz	Fastqsanger.gz
	SRR10417127_1.fastq.gz	Fastqsanger.gz
	SRR10417127_2.fastq.gz	Fastqsanger.gz
	SRR10417128_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Retinoic acid exerts disease stage-dependent effects on pristane-induced lupus

Project description:We previously showed that all-trans-retinoic acid (tRA), an active metabolite of vitamin A, exacerbated pre-existing autoimmunity in lupus; however, its effects before the development of autoimmunity are unknown. Here, using a pristane-induced model, we show that tRA exerts differential effects when given at the initiation vs. continuation phase of lupus. Unlike tRA treatment during active disease, pre-pristane treatment with tRA aggravated glomerulonephritis through increasing renal expression of pro-fibrotic protein laminin β1, activating bone marrow conventional dendritic cells (cDCs), and upregulating the interaction of ICAM-1 and LFA-1 in the spleen indicating an active process of leukocyte activation and trafficking. Transcriptomic analysis revealed that prior to lupus induction, tRA significantly upregulated the expression of genes associated with cDC activation and migration. Post-pristane tRA treatment, on the other hand, did not significantly alter the severity of glomerulonephritis; rather, it exerted immunosuppressive functions of decreasing circulatory and renal deposition of autoantibodies as well as suppressing the renal expression of proinflammatory cytokines and chemokines. Together, these findings suggest that tRA differentially modulate lupus-associated kidney inflammation depending on the time of administration. Interestingly, both pre- and post-pristane treatments with tRA reversed pristane-induced leaky gut and modulated the gut microbiota in a similar fashion, suggesting a gut microbiota-independent mechanism by which tRA affects the initiation vs. continuation phase of lupus.

2020-02-19 | GSE140104 | GEO

Retinoic Acid Exerts Disease Stage-Dependent Effects on Pristane-Induced Lupus.

Project description:We previously showed that all-trans-retinoic acid (tRA), an active metabolite of vitamin A, exacerbated pre-existing autoimmunity in lupus; however, its effects before the development of autoimmunity are unknown. Here, using a pristane-induced model, we show that tRA exerts differential effects when given at the initiation vs. continuation phase of lupus. Unlike tRA treatment during active disease, pre-pristane treatment with tRA aggravated glomerulonephritis through increasing renal expression of pro-fibrotic protein laminin β1, activating bone marrow conventional dendritic cells (cDCs), and upregulating the interaction of ICAM-1 and LFA-1 in the spleen, indicating an active process of leukocyte activation and trafficking. Transcriptomic analysis revealed that prior to lupus induction, tRA significantly upregulated the expression of genes associated with cDC activation and migration. Post-pristane tRA treatment, on the other hand, did not significantly alter the severity of glomerulonephritis; rather, it exerted immunosuppressive functions of decreasing circulatory and renal deposition of autoantibodies as well as suppressing the renal expression of proinflammatory cytokines and chemokines. Together, these findings suggest that tRA differentially modulate lupus-associated kidney inflammation depending on the time of administration. Interestingly, both pre- and post-pristane treatments with tRA reversed pristane-induced leaky gut and modulated the gut microbiota in a similar fashion, suggesting a gut microbiota-independent mechanism by which tRA affects the initiation vs. continuation phase of lupus.

| S-EPMC7103630 | biostudies-literature

Stage-dependent gene expression change in Sertoli cells regulated by retinoic acid signaling

Project description:To identifiy stage-dependent genes in Sertoli cells, we performed expression microarray analysis of the adult whole testes, cultured primary Sertoli cells, Sertoli cells directly isolated from wild-type and Nanos3 (germ-less) testes,seminiferous tubules at stages I-III, IV-VI, VII-VIII and IX-XII. Next to examine the relationship between stage-dependent gene expression change and retinoic acid signaling, we performed expression microarray analysis of the cultured primary Sertoli cells treated with retinoic acid and stage-specific seminiferous tubules injected with lentivirus containing Venus or dominat negative form of RARa, a dominant receptor for retinoic acid in Sertoli cells.

2012-07-01 | GSE34758 | GEO

Stage-dependent gene expression change in Sertoli cells regulated by retinoic acid signaling

2012-06-30 | E-GEOD-34758 | biostudies-arrayexpress

Immune-complex activated gasdermin D facilitates mitochondrial DNA membrane translocation and extracellular release in systemic lupus erythematous [RNA-Seq]

Project description:The purpose of this study was to study the roles of GSDMD in systemic lupus erythematous. Here, we used RNA sequencing from wild type, Pristane induced wild type and Pristane induced GSDMD knockout mice to detect changes in transcriptomes of kidneys.

2021-11-08 | GSE173767 | GEO

Whole blood gene expression profiles from a lupus nephritis mouse model: SNF1 (SWR X NZB F1) mice treated with pristane

Project description:We characterized the longitudinal gene expression profiles of whole blood from a novel lupus model nephritis: SNF1 (SWR X NZB F1) mice treated with pristane. Genes from interferon, plasma cell, neutrophil, T-cell and protein synthesis signatures were differentially expressed in the pristane-SNF1 model compared to the untreated matched control animals.

2016-09-06 | GSE86424 | GEO

NCF1-dependent low production of reactive oxygen species in plasmacytoid dendritic cells exacerbates lupus

Project description:Low capacity to produce reactive oxygen species (ROS) due to mutations in neutrophil cytosolic factor 1 (NCF1/p47phox) is strongly associated with lupus development both in humans and mouse models. Here, we aim to identify the major mechanisms of the Ncf1-disease association. We found that plasmacytoid dendritic cells (pDCs), the most potent producers of type I IFNs, exacerbate pristane-induced lupus in ROS-defective Ncf1-mutant and human NCF1-339 variant carrying mice. ROS deficiency in mouse models with Ncf1 mutation or human NCF1-339 variant leads to enhanced pDC generation via the TLR7/AKT/mTOR pathway and accumulation at sites of inflammation, resulting in an increased IFNα secretion. The produced IFNα further stimulates the JAK1/STAT1 pathway, which we found is hyperreactive in ROS-deficient pDCs. This, in turn, leads to increased type I IFN signature and enhanced proinflammatory responses. Our discoveries explain the causative effect of dysfunctional Ncf1 and pathogenicity of pDCs in lupus.

2023-03-12 | PXD035964 | Pride

Kidney gene expression profiles from a lupus nephritis mouse model: SNF1 (SWR X NZB F1) mice treated with pristane

Project description:We characterized the longitudinal gene expression profiles of kidneys from a novel lupus model nephritis: SNF1 (SWR X NZB F1) mice treated with pristane. 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 | GSE86425 | GEO

Zebrafish embryos treated with Retinoic Acid or Retinoic acid antagonist during gastrulation and early somitogenesis.

Project description:Retinoic acid (RA) is an important developmental signaling molecule responsible for the patterning of multiple vertebrate tissues. RA is also a potent teratogen, causing multi-organ birth defects in humans. Endogenous RA levels must therefore be tightly controlled in the developing embryo. In order to understand the RA function and regulation at the genomic level, we used a microarray approach to identify genes that function as negative feedback regulators of retinoic acid signaling. To that end, we treated embryos with different chemicals: DMSO as control, AGN193019 as RA antagonist at high concentration 10uM and low concentration 1uM, as well as 0.33uM RA. Each treatment has four biological replicates. We screened for genes expressed in early somite-stage embryos that respond oppositely to treatment with RA versus RA antagonists, and validated them by whole-mount RNA in situ hybridization.

2009-05-29 | GSE16264 | GEO

Transcriptomic analysis of Retinoic acid and 9 cis retinoic acid in zebrafish.

Project description:We are presenting the application of toxicogenomics in the evaluation of the toxic effects of retinoic acid and one of its isoforms the 9-cis retinoic acid. The main goal is to distinguish the pattern of action of the both chemical compounds and their action in an extended exposure. The results suggest a different pattern within the days and the chemicals. Representatives of each GO functional groups were selected and quantified by real-time PCR to validate the microarray data and to differentiate the action of retinoic acid compounds studied.

2015-12-31 | GSE41335 | GEO

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