Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27677993.fastq.gz | Fastqsanger.gz | |||
| SRR27677994.fastq.gz | Fastqsanger.gz | |||
| SRR27677995.fastq.gz | Fastqsanger.gz | |||
| SRR27677996.fastq.gz | Fastqsanger.gz | |||
| SRR27677997.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:DDR2 regulates genes in MSCs and in MDA-MD-231 cells primed with MSCs
2016-12-17 | GSE92485 | GEO
Project description:Background: Non-healing wounds cause profound suffering of patients and a huge economic burden on society. Current research attempts to refine MSC-based therapies for this type of difficult-to-treat wounds. We earlier reported that injection of S100A8/A9 primed MSCs into the wound edge in mice accelerates wound healing compared to non-primed MSCs. We here describe a protective response of differentially expressed isoforms of genes, proteins and their potential role in the reported beneficial effects of S100A8/A9 primed MSCs on tissue repair. Methods: Adipose‐derived MSCs were characterized for specific cell surface markers using flow cytometry and assessed for their ability to differentiate into different lineages. To further investigate the mechanisms underlying the beneficial effects of S100A8/A9 primed MSCs, we employed a multi‐omics strategy that combined transcriptome, secretome, and proteome analyses. Global translational activity and a potential metabolic shift were examined using fluorescent labeling alongside seahorse‐based metabolic assays. Additionally, in silico analysis was conducted to assess the presence of the DRACH motif in mRNAs encoding these proteins, thereby evaluating their potential for cap-independent, m6A‐mediated translation. Results: Enhanced protein translation was observed in MSCs primed with S100A8/A9. Priming significantly increased the levels of the cap-independent translation initiation factor EIF3I, while reducing the cap-dependent factor EIF4A1, suggesting a shift in the mode of translation. In addition, the secretome of S100A8/A9-primed MSCs exhibited upregulation of cystatin C, a tissue protective protease inhibitor, and angiopoietin-1, an inducer of angiogenesis. Furthermore, various collagens, which serve as MSC niche-protecting proteins, were expressed at higher levels in the S100A8/A9 primed MSCs. Notably, the mRNAs corresponding to these factors contained DRACH motifs. Conclusion: We uncovered a protective response in S100A8/A9 primed MSCs that alters translation processes and increases the secretion of protective proteins, whose functions warrant further exploration. In the long term, S100A8/A9 priming holds promise for developing more effective MSC‐based therapies to enhance wound healing.
2026-06-09 | GSE301531 | GEO
Project description:To compare the expression profile of extracellular vesicles/exosomes derived from naïve and bioglass-primed human adipose tissue-derived MSCs
2025-04-12 | GSE200740 | GEO
Project description:Intrauterine adhesion (IUA), characterized by endometrial fibrosis, is a common cause of female reproductive disorders. IUA-like mice model was created with curettage plus LPS stimulation to mimic endometrial fibrosis in IUA patients. Mesenchymal stem cells (MSCs) based therapy is applied to some refractory immune diseases to control inflammation and their immunomodulatory function can be enhanced via pre-treatment with inflammatory cytokines. In this work, we examined the effect of untreated and cytokines primed MSCs therapy on macrophage in IUA-like mice model. The uteri samples were collected from sham, IUA modeling, IUA+control MSCs treatment and IUA+primed MSCs treatment groups of mice. Endometrial macrophages were sorted through F4/80 magnetic beads and performed RNA-seq.
2023-06-12 | GSE224288 | GEO
Project description:Mesenchymal stem-cells (MSCs) are of particular interest for treating immune-related diseases due to their immunosuppressive capacities. Here, we show that Small sized MSCs primed with Hypoxia and Calcium ion (SHC-MSCs) exhibit the enhanced functions regarding stemness and immunomodulation for treating allogeneic conflicts. Compared with naïve cultured human umbilical cord-blood MSCs, SHC-MSCs were resistant to the passage dependent cellular senescence mediated by MCP-1 and p53/p21 cascade and highly secreted the pro-angiogenic and immune-modulatory factors, resulting in suppression of T-cell proliferation. Genome-wide DNA methylome and transcriptome analysis indicate that SHC-MSCs characteristically up-regulated immune-modulation, cell adhesion and cell-cycle related genes. As downstream factors, PLK1, ZNF143, DHRS3, and FOG2 proteins played a key role on the beneficial effects of SHC-MSCs, evidenced by the promoted self-renewal, migration, pro-angiogenic, anti-inflammatory, and T cell suppression capacities in their-over-expressing MSCs. Importantly, administration of SHC-MSCs or PLK1-over-expressing cells (PLK1-MSCs) significantly reduced the symptoms of graft-versus-host disease (GVHD) in a humanized mouse model which led to significantly improved survival, less weight loss, and less histopathologic injuries of GVHD target organs compared with naive MSC-infused mice. Collectively, our study suggests that small-sized MSCs primed with hypoxia could advance the therapeutic strategy for the clinical treatment of allogeneic conflicts including GVHD.
2018-08-01 | GSE108563 | GEO
Project description:Mesenchymal stem-cells (MSCs) are of particular interest for treating immune-related diseases due to their immunosuppressive capacities. Here, we show that Small sized MSCs primed with Hypoxia and Calcium ion (SHC-MSCs) exhibit the enhanced functions regarding stemness and immunomodulation for treating allogeneic conflicts. Compared with naïve cultured human umbilical cord-blood MSCs, SHC-MSCs were resistant to the passage dependent cellular senescence mediated by MCP-1 and p53/p21 cascade and highly secreted the pro-angiogenic and immune-modulatory factors, resulting in suppression of T-cell proliferation. Genome-wide DNA methylome and transcriptome analysis indicate that SHC-MSCs characteristically up-regulated immune-modulation, cell adhesion and cell-cycle related genes. As downstream factors, PLK1, ZNF143, DHRS3, and FOG2 proteins played a key role on the beneficial effects of SHC-MSCs, evidenced by the promoted self-renewal, migration, pro-angiogenic, anti-inflammatory, and T cell suppression capacities in their-over-expressing MSCs. Importantly, administration of SHC-MSCs or PLK1-over-expressing cells (PLK1-MSCs) significantly reduced the symptoms of graft-versus-host disease (GVHD) in a humanized mouse model which led to significantly improved survival, less weight loss, and less histopathologic injuries of GVHD target organs compared with naive MSC-infused mice. Collectively, our study suggests that small-sized MSCs primed with hypoxia could advance the therapeutic strategy for the clinical treatment of allogeneic conflicts including GVHD.
2018-08-01 | GSE108562 | GEO
Project description:Mesenchymal stem cells (MSCs) exist in almost all tissues and participate in tissue regeneration and homeostasis. MSCs based therapy is applied to some refractory immune diseases to control inflammation, such as lupus nephritis, Crohn’s disease and rheumatoid arthritis. However, accumulating studies showed that the immunomodulatory capacity of naïve MSCs is mild and limited. To enhance MSCs immunomodulatory function, researchers innovated a new method to reprogram MSCs via pre-treatment with inflammatory cytokines. In this work, we firstly used a cocktail of three cytokines, IL-1β, TNF-a and IFN-γ, to treat hUC-MSCs (human MSCs from umbilical cord). We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 untreated hUC-MSCs (ctrl) and 3 cytokines-treated hUC-MSCs (primed).
2023-06-12 | GSE224190 | GEO
Project description:Therapeutic mesenchymal stromal cells (MSCs) are used to support the healing of severe injuries such as skin burn wounds. However, the pivotal expansion from donor biopsies on conventionally stiff culture surfaces activates MSCs into scar-promoting myofibroblasts. We previously coined the term mechanical memory to describe that priming of MSCs on scar-stiff culture substrates imprints myofibroblast features that persist even after a switch to skin-soft substrates. We now unravel mechanisms and factors that, conversely, suppress myofibroblast activation upon priming in skin-soft expansion culture. Such ‘soft memory’ factors are poised to preserve MSC regenerative features while suppressing fibrogenesis. Mechanically primed MSCs were compared by RNA- and assay for transposase-accessible chromatin (ATAC)-sequencing. The promoters of genes that were highly accessible and upregulated upon soft priming and memorized after switch to stiff substrates were significantly enriched for motifs predicted to bind the transcription factor HOXA11. Knockdown of HOXA11 resulted in enhanced expression of fibrogenic and osteogenic genes in soft-primed MSCs and reduced expression of anti-fibrotic factors, including the transcription factor SALLl1. SALL1 is a potent suppressor of pro-fibrotic genes such as Postn, Col8a1, Grem2, Thps1 and Thps2, and the transcription factor Gata6. GATA6, in turn, emerges as a keeper of stiff-induced myofibroblast memory by maintaining the accessibility of pro-fibrotic genes even after switch to soft substrates. By manipulating the SALL1-GATA6 transcriptional circuit in culture, we produced therapeutic MSCs that suppress fibrosis in an animal model of hypertrophic skin scarring. We propose that similar control over myofibroblast memory will enhance the success of therapeutic MSC applications in organ repair.
2026-04-09 | GSE310502 | GEO
Project description:We here addressed the question whether the unique capacity of mesenchymal stromal/stem cells (MSCs) to re-establish tissue homeostasis depends on their potential to sense pathogen associated molecular pattern (PAMP) and, in consequence, mount an adaptive response in the interest of tissue repair. After injection of MSCs which had been primed with the bacterial wall component LPS into murine wounds, an unexpected acceleration of healing occurred, clearly exceeding that of non-primed MSCs. This correlates with a fundamental reprogramming of the transcriptome in LPS treated MSCs as deduced from RNA-seq analysis and its validation. A network of genes mediating the adaptive response through the TLR-4 pathway responsible for neutrophil activation (GCP- 2, ENA-78, IL-1β IL-8) and MSC protection (SOX6) profoundly contributes to enhanced wound healing. In fact, silencing of either TRL-4, or IRAK3, a downstream effector of TRL-4, or SOX6 suppressed wound healing most likely due to suppression of neutrophil extracellular trap formation and suppression of the enhanced microbicidal release of reactive oxygen species (ROS), key features of neutrophil activation. This previously unreported results uncover SOX6 which protects MSCs at the wound site from enhanced oxidative stress. This unprecedented findings hold substantial promise to refine current MSC-based therapies for difficult-to-treat wounds.
2018-05-09 | GSE114189 | GEO
Project description:Therapeutic mesenchymal stromal cells (MSCs) are used to support the healing of severe injuries such as skin burn wounds. However, the pivotal expansion from donor biopsies on conventionally stiff culture surfaces activates MSCs into scar-promoting myofibroblasts. We previously coined the term mechanical memory to describe that priming of MSCs on scar-stiff culture substrates imprints myofibroblast features that persist even after a switch to skin-soft substrates. We now unravel mechanisms and factors that, conversely, suppress myofibroblast activation upon priming in skin-soft expansion culture. Such ‘soft memory’ factors are poised to preserve MSC regenerative features while suppressing fibrogenesis. Mechanically primed MSCs were compared by RNA- and assay for transposase-accessible chromatin (ATAC)-sequencing. The promoters of genes that were highly accessible and upregulated upon soft priming and memorized after switch to stiff substrates were significantly enriched for motifs predicted to bind the transcription factor HOXA11. Knockdown of HOXA11 resulted in enhanced expression of fibrogenic and osteogenic genes in soft-primed MSCs and reduced expression of anti-fibrotic factors, including the transcription factor SALLl1. SALL1 is a potent suppressor of pro-fibrotic genes such as Postn, Col8a1, Grem2, Thps1 and Thps2, and the transcription factor Gata6. GATA6, in turn, emerges as a keeper of stiff-induced myofibroblast memory by maintaining the accessibility of pro-fibrotic genes even after switch to soft substrates. By manipulating the SALL1-GATA6 transcriptional circuit in culture, we produced therapeutic MSCs that suppress fibrosis in an animal model of hypertrophic skin scarring. We propose that similar control over myofibroblast memory will enhance the success of therapeutic MSC applications in organ repair.
2026-04-09 | GSE310514 | GEO