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The X-linked chromatin modifier SMC1A is deregulated in lupus female monocytes and promotes autoimmunity [RNA-Seq]

ABSTRACT: The X-linked chromatin modifier SMC1A is deregulated in lupus female monocytes and promotes autoimmunity [RNA-Seq]

PROVIDER: PRJNA1174162 | ENA |

REPOSITORIES: ENA

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The X-linked chromatin modifier SMC1A is deregulated in lupus female monocytes and promotes autoimmunity [RNA-Seq]

Project description:Biological sex underlines the onset of autoimmunity yet the underlying molecular mechanisms remain ill-defined. Female susceptibility is prominent in systemic lupus erythematosus (SLE), an autoimmune disease of substantial burden. Herein we demonstrate that SMC1A, a subunit of the cohesin complex that escapes X-chromosome inactivation, exhibits female-biased expression in monocytes from SLE patients and those cultured under lupus-inducing stimulus. By altering SMC1A dosage, the expression of immune-related genes, particularly those responsive to lupus environment, was affected. Active enhancers of immune and inflammatory pathways showed widespread SMC1A redistribution in lupus-like monocytes, as revealed by integrated analysis of SMC1A binding, chromatin activity and accessibility. Our data support SMC1A as a sex-biased chromatin modifier that enhances inflammatory responses in lupus.

2025-09-01 | GSE279728 | GEO

The X-linked chromatin modifier SMC1A is deregulated in lupus female monocytes and promotes autoimmunity [ChIP-Seq]

2025-09-01 | GSE279726 | GEO

The X-linked chromatin modifier SMC1A is deregulated in lupus female monocytes and promotes autoimmunity [ChIP-Seq]

Project description:The X-linked chromatin modifier SMC1A is deregulated in lupus female monocytes and promotes autoimmunity [ChIP-Seq]

| PRJNA1174160 | ENA

SMC1A ChIP-seq in primary human keratinocytes

Project description:This study examines the DNA binding regions of SMC1A, a subunit of the Cohesin complex, in undifferentiated human keratinocytes.

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Gene expression data of human keratinocytes knocked down for SMC1A, SMC3, or control shRNA.

Project description:The purpose of the study is to understand the impacts of cohesin knockdown on epidermal gene expression. Primary human keratinocytes were knocked down for SMC1A, SMC3, or control to determine its genome-wide gene expression profile. Global gene expression profiling using U133 plus 2.0 arrays were used to deteremine the genes perturbed by knockdown of SMC1A or SMC3.

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Uncovering Modifier Genes of X-linked Alport Syndrome Using a Novel Multi-parent Mouse Model

Project description:RNAseq of mouse kidney RNA from Col4a5 muntant mice crossed with diversity ourbred mice to find modifier genes of Alport disease.

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SMC1A, CTCF and MITF level on chromatin after knockdown of NIPBL in melanoma cell line

Project description:SMC1A, CTCF and MITF level on chromatin was studied after knockdown of NIPBL in 501mel

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Microbiota-derived Inosine Suppresses Systemic Autoimmunity via Restriction of B Cell Differentiation and Migration

Project description:The role of gut microbiota dysbiosis in systemic lupus erythematosus (SLE) pathogenesis remains elusive. Here, we show that fecal microbiota transplantation (FMT) from healthy mice to lupus mice ameliorated lupus-like symptoms. Microbiota reconstitution effectively reduced systemic class switch recombination and elevated IGH naïve isotype. Microbiota profiling revealed an enrichment of Lactobacillus johnsonii post-FMT, with a significant correlation to purine metabolites. Importantly, the Lactobacillus johnsonii-derived inosine, an intermediate metabolite in purine metabolism, effectively alleviated lupus-like symptoms by impeding B cell differentiation and reducing renal B cell infiltration. We further demonstrated that inosine reprograms B cells through the ERK-HIF-1α signaling pathway. Overall, our study highlights the discovery of a novel microbial metabolite modulating autoimmunity and suggests its potential for innovative microbiome-based therapeutic approaches.

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Loss of Trex1 in dendritic cells is sufficient to trigger systemic autoimmunity

Project description:Biallelic defects of the gene encoding for the intracellular enzyme 3â repair exonuclease (Trex)1 cause Aicardi-GoutiÃ¨res syndrome (AGS), a rare monogenic, lupus-like autoimmune disease, while heterozygous Trex1 loss of function alleles are associated with systemic lupus erythematosus (SLE). Trex1-/- mice develop lethal autoimmune multi-organ inflammation, which results from a chronic type I IFN response triggered by intracellular accumulation of a putative nucleic acid substrate of Trex1. This pathogenic nucleic acid is detected by the broadly, but not ubiquitously, expressed cytosolic DNA sensor cGAS, raising the question whether there are specific cell types that respond to Trex1 deficiency by production of IFN and induce autoimmunity. We generated mice with conditional knock out of the Trex1 gene and demonstrated that loss of Trex1 throughout the hematopoietic system and even selective loss in dendritic cells is sufficient to cause IFN release and autoimmunity. B cells showed no transcriptional response to Trex1 deficiency. Trex1-/- keratinocytes produced IFN but did not induce skin inflammation, whereas loss of Trex1 in cardiomyocytes triggered neither IFN response nor pathology. Trex1-deficient neurons and astrocytes did not release IFN in the CNS. In contrast, mice with selective inactivation of Trex1 in long-living CNS macrophages such as microglia locally produced IFN but did not reproduce the mild encephalitis seen in Trex1-/- mice. Collectively, individual cell types differentially respond to the loss of Trex1 and dendritic cells seem promising candidates for experiments addressing the molecular pathomechanism in Trex1 deficiency. We sorted CD19-positive B cells from spleens of Trex1fl/fl CD19-Cre+ and Trex1fl/fl CD19-Cre- mice and isolated total RNA for library construction to perform mRNA deep sequencing.

2016-08-01 | E-GEOD-77693 | biostudies-arrayexpress

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2019-03-19 | GSE128453 | GEO

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