Interferon Regulatory Factor 7 (IRF7) in aging of adipose-derived mesenchymal stromal cells
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PROVIDER: PRJNA708218 | ENA |
REPOSITORIES: ENA
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Project description:We found that Interferon Regulatory Factor 7 (IRF7) is upregulated in adipose-derived stromal cells (MSC) of 12 months-old (middle-age) mice compared with 1 month-old mice. To go in depth into the role of IRF7 in aging of MSC we knocked-down it in 12 months MSC and assessed the transcriptional changes though whole-genome microarray analysis. We investigated the transcriptional changes induced by the Interferon Regulatory Factor 7 (IRF7) knock-down in mesenchymal stromal cells established from the inguinal fat pad of 12-months-old mice.
2021-03-10 | GSE168533 | GEO
Project description:Interferon Regulatory Factor 7 (IRF7), and its homologue IRF3, are master transcriptional regulators of the innate immune response. IRF7 binds to promoters of interferon beta (IFNb) and several IFNas, as a homodimer or as a heterodimer with IRF3 to drive expression of these type I IFNs, which in turn activate additional signaling pathways to promote expression of anti-viral genes. Here we demonstrate that retention of the first intron within the coding region of IRF7 is highly regulated across immune tissues and in response to viral infection and other immunologic signals. Importantly, retention of this intron generates an alternative translation start site, resulting in a N-terminally extended form of the protein (exIRF7). Using CRISPR gene editing to generate cells that only express exIRF7, or the canonical version of IRF7 (cIRF7), we demonstrate that exIRF7 uniquely activates a program of genes, including IFNb, in response to innate immune triggers. We conclude that alternative splicing of IRF7 is a previously unrecognized mechanisms used by human cells to tune the interferon response to viral infection and other immune challenges.
2025-07-17 | GSE285352 | GEO
Project description:Single-cell sequencing of adipose-derived mesenchymal stromal cells and fibroblasts.
| EGAS00001006954 | EGA
Project description:Human adipose mesenchymal stromal cells cutltured in culture media containing diabetic patient serum or normal indvidual serum as control for 6 days and 1 month period
2024-06-22 | PXD036116 | Pride
Project description:Alternate isoforms of IRF7 Differentially Regulate Interferon Expression
| PRJNA1203213 | ENA
Project description:Intron retention (IR) has emerged as an important mechanism of gene expression control. Despite this, the factors that control IR events remain poorly understood. We observed consistent IR in one intron of the Irf7 gene and identified Bud13 as an RNA-binding protein that acts at this intron to increase the amount of successful splicing. Deficiency in Bud13 led to increased IR, decreased mature Irf7 transcript and protein levels, and consequently to a dampened type I interferon response. This impairment of Irf7 production in Bud13 deficient cells compromised their ability to withstand VSV infection. Global analysis of Bud13 knockdown and BUD13 cross-linking to RNA revealed a subset of introns that share many characteristics with the one found in Irf7 and are spliced in a Bud13-dependent manner. Deficiency of Bud13 led to decreased mature transcript from genes containing such introns. Thus, by acting as an antagonist to IR, Bud13 facilitates the expression of genes at which IR occurs.
2018-11-15 | GSE122543 | GEO
Project description:Background Lymphedema, a chronic and progressive disease, is characterized by lymphatic dysfunction, persistent inflammation, fibrosis, and pathological adipose tissue remodeling. Although adipose-derived stromal cells (ASCs) are implicated in disease progression, the stromal cell states and stromal–immune interactions that sustain chronic fibro-inflammatory remodeling remain poorly defined. Methods Single-cell RNA sequencing was performed of the stromal vascular fraction isolated from anatomically matched human subcutaneous adipose tissues. These tissues were obtained from patients with advanced-stage lymphedema and healthy individuals to delineate disease-associated stromal heterogeneity at single-cell resolution. Results A disease-expanded ASC progenitor population (ASC_c2) that exhibits pronounced transcriptional reprogramming in lymphedema was identified. The ASC_c2 population segregated into two mutually exclusive pathological subsets: a VCAM1⁺ vascular-interacting stromal population (V-ASCs) associated with ECM remodeling and CD74⁺HLA class II–expressing subset (I-ASCs) with antigen-presentation-like features. I-ASCs displayed a robust interferon-responsive transcriptional program consistent with immune priming and preferentially expressed the CXCL14 chemokine. Ligand–receptor interaction analysis revealed biased stromal–immune interactions between I-ASCs and CD8⁺ T cells, suggesting a skewed immune microenvironment in lymphedematous adipose tissue. Conclusions Our findings suggest an immune-skewed stromal–immune axis in lymphedema, driven by immune-primed, antigen-presentation-like ASCs. The study findings suggest a cellular framework linking stromal reprogramming to chronic immune dysregulation and fibrosis in human lymphedema, offering insights into potential therapeutic targets for interrupting pathological stromal–immune crosstalk.
2026-04-17 | GSE327961 | GEO
Project description:Adipose stromal cells are adipocytes progenitors lying in the stroma vascular fraction of adipose tissue. They can also be released into the circulation upon dietary challenges. We used microarrays to compare the global programme of gene expression between adipose stromal cells originating from murine subcutaneous and perigonadal adipose depots
2019-04-04 | GSE127928 | GEO
Project description:Toll-like receptor 7 (Tlr7) deficiency-accelerated severe COVID-19 is associated with reduced production of interferons (IFNs). However, the underlying mechanisms remain elusive. Here, we demonstrate that the deficiency of Tlr7 and Irf7 globally and/or in immune cells in mice increases the severity of COVID-19 via impaired IFN activation in both immune and/or non-immune cells, leading to increased lung viral loads. These effects are associated with reduced IFN alpha and gamma production. The deficiency of Tlr7 in the infected mice tends to cause the reduced production and nuclear translocation of Interferon regulatory factor 7 (IRF7), indicative of reduced IRF7 activation. Despite higher amounts of lung viral antigen, Tlr7 or Irf7 deficiency resulted in substantially reduced production of antibodies against SARS-CoV-2, thereby delaying the viral clearance. These results highlight the importance of the activation of TLR7 and IRF7, leading to IFN production on the development of innate and adaptive immunity against COVID-19.
2024-09-05 | GSE274586 | GEO
Project description:Toll-like receptor 7 (Tlr7) deficiency-accelerated severe COVID-19 is associated with reduced production of interferons (IFNs). However, the underlying mechanisms remain elusive. Here, we demonstrate that the deficiency of Tlr7 and Irf7 globally and/or in immune cells in mice increases the severity of COVID-19 via impaired IFN activation in both immune and/or non-immune cells, leading to increased lung viral loads. These effects are associated with reduced IFN alpha and gamma production. The deficiency of Tlr7 in the infected mice tends to cause the reduced production and nuclear translocation of Interferon regulatory factor 7 (IRF7), indicative of reduced IRF7 activation. Despite higher amounts of lung viral antigen, Tlr7 or Irf7 deficiency resulted in substantially reduced production of antibodies against SARS-CoV-2, thereby delaying the viral clearance. These results highlight the importance of the activation of TLR7 and IRF7, leading to IFN production on the development of innate and adaptive immunity against COVID-19.
2024-08-20 | GSE274686 | GEO