ARID3a expression in human hematopoietic stem cells is associated with distinct gene patterns in aged individuals
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ABSTRACT:
PROVIDER: PRJNA576353 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10243100_1.fastq.gz | Fastqsanger.gz | |||
| SRR10243100_2.fastq.gz | Fastqsanger.gz | |||
| SRR10243200_1.fastq.gz | Fastqsanger.gz | |||
| SRR10243200_2.fastq.gz | Fastqsanger.gz | |||
| SRR10243300_1.fastq.gz | Fastqsanger.gz |
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Project description:Aging results in altered gene expression patters in HSCs expressing ARID3A transcirpts, with a number of genes downregulated in aged donor ARID3a+ HSCs compared to young donor ARID3a+ HSCs
2020-08-03 | GSE138544 | GEO
Project description:BackgroundImmunologic aging leads to immune dysfunction, significantly reducing the quality of life of the elderly. Aged-related defects in early hematopoiesis result in reduced lymphoid cell development, functionally defective mature immune cells, and poor protective responses to vaccines and pathogens. Despite considerable progress understanding the underlying causes of decreased immunity in the elderly, the mechanisms by which these occur are still poorly understood. The DNA-binding protein ARID3a is expressed in a subset of human hematopoietic progenitors. Inhibition of ARID3a in bulk human cord blood CD34+ hematopoietic progenitors led to developmental skewing toward myeloid lineage at the expense of lymphoid lineage cells in vitro. Effects of ARID3a expression in adult-derived hematopoietic stem cells (HSCs) have not been analyzed, nor has ARID3a expression been assessed in relationship to age. We hypothesized that decreases in ARID3a could explain some of the defects observed in aging.ResultsOur data reveal decreased frequencies of ARID3a-expressing peripheral blood HSCs from aged healthy individuals compared with young donor HSCs. Inhibition of ARID3a in young donor-derived HSCs limits B lineage potential, suggesting a role for ARID3a in B lymphopoiesis in bone marrow-derived HSCs. Increasing ARID3a levels of HSCs from aged donors in vitro alters B lineage development and maturation. Finally, single cell analyses of ARID3a-expressing HSCs from young versus aged donors identify a number of differentially expressed genes in aged ARID3A-expressing cells versus young ARID3A-expressing HSCs, as well as between ARID3A-expressing and non-expressing cells in both young and aged donor HSCs.ConclusionsThese data suggest that ARID3a-expressing HSCs from aged individuals differ at both molecular and functional levels compared to ARID3a-expressing HSCs from young individuals.
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Project description:In order to determine proteins interacting with ARID3A in the ML-DS cell line CMK, we performed CoIP of endogenous ARID3A followed by LC-MS/MS
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Project description:Methyl-seq data was obtained from total peripheral blood mononuclear cells of two patients with systemic lupus erythematosus who were characterized as having>2 standard deviations more ARID3a-expressing B lymphocytes than healthy controls. Similarly, methyl-seq data was also obtained from two SLE patient samples with normal (low) numbers of ARID3-expressing B lymphocytes. Our previous studies showed that increased ARID3a expression in B lymphocytes was associated increased disease activity. Data were generated on an Illumina Hiseq 2000 with paired-end 100bp reads and quality control metrics were assessed with Picard tools. Methylation profiles of genomic DNA from four SLE patient PBMC samples, two with high numbers of ARID3a expressing B cells (ARID3aH) versus two with normal numbers of ARID3a+ B cells (ARID3aN), were generated on an Illumina Hiseq 2000 with paired-end 100bp reads.
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Project description:Previous studies in the mouse indicated that Arid3a plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that Arid3a is widely expressed during mouse and human placentation and essential for early embryonic viability. Arid3a is located within trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with sever defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in inflammatory response-related genes, cytokines and chemokines. We provide evidence that BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent (iPS) stem cells results in ARID3A upregulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in human iPS and BMP4-mediated TS-like cells up-regulated TE markers, whereas pluripotent markers were down-regulated. Our results indicate that the roles of Arid3a are conserved and essential for mammalian placental development through regulation of both intrinsic and extrinsic developmental programs. Placentas of E10.5 and E11.5 wild type (WT) and Arid3a-/- mice were generated by deep sequencing, using Illumina
2016-07-01 | E-GEOD-79638 | biostudies-arrayexpress
Project description:Previous studies in the mouse indicated that Arid3a plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that Arid3a is widely expressed during mouse and human placentation and essential for early embryonic viability. Arid3a is located within trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with sever defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in inflammatory response-related genes, cytokines and chemokines. We provide evidence that BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent (iPS) stem cells results in ARID3A upregulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in human iPS and BMP4-mediated TS-like cells up-regulated TE markers, whereas pluripotent markers were down-regulated. Our results indicate that the roles of Arid3a are conserved and essential for mammalian placental development through regulation of both intrinsic and extrinsic developmental programs.
2016-07-01 | GSE79638 | GEO
Project description:Methyl-seq data was obtained from total peripheral blood mononuclear cells of two patients with systemic lupus erythematosus who were characterized as having>2 standard deviations more ARID3a-expressing B lymphocytes than healthy controls. Similarly, methyl-seq data was also obtained from two SLE patient samples with normal (low) numbers of ARID3-expressing B lymphocytes. Our previous studies showed that increased ARID3a expression in B lymphocytes was associated increased disease activity. Data were generated on an Illumina Hiseq 2000 with paired-end 100bp reads and quality control metrics were assessed with Picard tools.
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Project description:To test the function and regulated genes of ARID3A gene, we conducted lentivirus-mediated short hairpin RNA (shRNA) against ARID3A in K562 cell line.
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Project description:Percentages of ARID3a-expressing low density neutrophils in SLE patients correlate with lupus disease activity and Type I IFN production. ARID3a protein levels also correlate with interferon expression in plasmacytoid dendritic cells. Gene profiles mechanistically link ARID3a with inflammatory pathway regulation.
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Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification. Arid3a overexpression and Arid3a knockdown Total RNA was isolated from cultured cells using RNeasy plus mini kit (Qiagen). cDNA were synthesized and labelled, followed by hybridization on Affymetrix GeneChip mouse genome 430A 2.0 arrays.
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