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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Project description:DDR2 regulates genes in MSCs and in MDA-MD-231 cells primed with MSCs
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Project description:To compare the expression profile of extracellular vesicles/exosomes derived from naïve and bioglass-primed human adipose tissue-derived MSCs
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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: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:The gene expression of bone marrow cells of mice enriched for Gremlin1 vs control was measured (n=3). It is not known if endogenous adult mesenchymal stem cells (MSCs) exist.Following culture,perisinusoidal mesenchymal cells can clonally recapitulate the skeletal microenvironment, but this fails to confirm their endogenous lineage repertoire. Multipotential MSCs in vitro may be fate-restricted in vivo and specific perisinusoidal recombination does not trace bone or cartilage Reconciling in vitro MSCs with their in vivo potential has been challenging and remains untested outside of the bone. We prove that expression of the bone morphogenetic protein (BMP)-antagonist gremlin 1 (Grem1) identifies a population of self-renewing, multipotent bone, cartilage and stromal-primed MSCs in both health and healing that are completely distinct from the established Nes-GFP niche-supporting mesenchymal cells. Grem1 recombination also identifies small intestinal MSCs (siMSCs) that can be transplanted and clonally trace the self-renewing, multilineage periepithelial mesenchymal sheath. Our findings prove the existence of adult MSCs that are regionally and functionally distinct from perisinusoidal Nes-GFP cells. We also established that the mesenchyme undergoes ordered turnover outside of the bone and may help to preserve regional niches. Grem1 MSCs provide a new focus for investigating mesenchymal renewal and repair. a.Adult (6-8 weeks) Grem1;TdTomato mice were induced by oral tamoxifen and their bone marrow harvested by digestion sorted for Non-recombined CD45/CD31/Ter-119 triple negative bone marrow cells (n=3). b.Adult (6-8 weeks) Grem1;TdTomato mice were induced by oral tamoxifen and their bone marrow harvested by digestion sorted for Grem1 (n=3). Same mice as in a so that samples are matched.
2015-02-10 | E-GEOD-57729 | biostudies-arrayexpress
Project description:The gene expression of bone marrow cells of mice enriched for Gremlin1 vs control was measured (n=3). It is not known if endogenous adult mesenchymal stem cells (MSCs) exist.Following culture,perisinusoidal mesenchymal cells can clonally recapitulate the skeletal microenvironment, but this fails to confirm their endogenous lineage repertoire. Multipotential MSCs in vitro may be fate-restricted in vivo and specific perisinusoidal recombination does not trace bone or cartilage Reconciling in vitro MSCs with their in vivo potential has been challenging and remains untested outside of the bone. We prove that expression of the bone morphogenetic protein (BMP)-antagonist gremlin 1 (Grem1) identifies a population of self-renewing, multipotent bone, cartilage and stromal-primed MSCs in both health and healing that are completely distinct from the established Nes-GFP niche-supporting mesenchymal cells. Grem1 recombination also identifies small intestinal MSCs (siMSCs) that can be transplanted and clonally trace the self-renewing, multilineage periepithelial mesenchymal sheath. Our findings prove the existence of adult MSCs that are regionally and functionally distinct from perisinusoidal Nes-GFP cells. We also established that the mesenchyme undergoes ordered turnover outside of the bone and may help to preserve regional niches. Grem1 MSCs provide a new focus for investigating mesenchymal renewal and repair.
2015-02-10 | GSE57729 | GEO