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Regenerating Skeletal Muscle of Ovariectomized Mice

ABSTRACT: In this study, we found more stable Siglec1 expression and stronger CD169+ macrophage staining in the muscle of 17-β-estradiol-treated mice than in that of the placebo-treated mice. However, Siglec1 was correlated with more interferon-related genes in the muscle of the placebo-treated mice. These findings suggest that Siglec1/IFN1 activity may be part of the inflammatory response during muscle regeneration. Future studies are warranted to investigate this role.

ORGANISM(S): Mus musculus

PROVIDER: GSE311704 | GEO | 2025/12/19

REPOSITORIES: GEO

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Regenerating Skeletal Muscle of Ovariectomized Mice

Project description:Regenerating Skeletal Muscle of Ovariectomized Mice

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Analysis of aortic gene expression in ovariectomized ApoE-deficient mice substituted with medroxyprogesterone acetate, norethisterone acetate or placebo

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Analysis of aortic gene expression in ovariectomized ApoE-deficient mice substituted with medroxyprogesterone acetate, norethisterone acetate or placebo

Project description:Agilent 4x44k Whole Mouse Genome v1 Microarrays were used to analyze aortic transcriptome of mice substituted with medroxyprogesterone acetate, norethisterone acetate or placebo after having been ovariectomized. The aim of this experiment was to detect genes regulated in the gestagen-treated groups as compared to placebo that might be involved in thrombotic events Aortic gene expression was analyzed in ApoE-deficient mice after ovariectomy and 90 days of hormone- or placebo-treatment (medroxyprogesterone acetate or norethisterone acetate) and feeding a high-fat Western-type diet.

2014-06-30 | E-GEOD-57972 | biostudies-arrayexpress

Single-cell transcriptome analysis reveals atypical monocytes circulating ahead of acute graft-versus-host disease clinical onset

Project description:Acute graft-versus-host disease (aGVHD) represents the rejection of the skin, gut and liver tissues of the recipient of an allogenic hematopoietic stem cell transplantation (HSCT) by the donor T-cells. The onset of aGVHD is often rapid and its evolution unpredictable. We undertook the single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) collected before aGVHD clinical onset in three patients and at aGVHD diagnosis in one, using four HSCT recipients who remained free of aGVHD as controls. This analysis unveiled the presence in the circulation of particular subpopulations of monocytes and cytotoxic T cells (CTLs) in pre-aGVHD samples up to 18 days before clinical disease. These pre-aGVHD monocytes were characterized by an upregulation of the M2 polarity marker CD163, and the transmembrane protein SIGLEC1/CD169, while their CTL counterparts stood out for the upregulation of the CXCL10 receptor CXCR3 and the antigenic stimulation marker CD70. The occurrence of CD163/CD169-co-expressing monocytes upstream of aGVHD onset was validated using RNAseq data from an independent cohort and by flow cytometry of blood samples. These findings point to potential early diagnostic tools and preventive therapeutic strategies for aGVHD.

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HDAC inhibitors promote the pro-myogenic activity of Sca1-positive interstitial cells in regenerating dystrophic muscles

Project description:We report here on the identification and functional characterization of Sca1-positive muscle interstitial cells that contribute to regeneration or fibroadipogenic degeneration of dystrophic muscles and mediate the beneficial effects of HDAC inhibitors (HDACi) in mdx mice. We found that the phenotype adopted by these cells and their biological activity are influenced by changes in muscle environment. While Sca1-positive muscle interstitial cells from healthy muscles spontaneously adopt a fibro-adipogenic phenotype, Sca1-positive muscle interstitial cells isolated from dystrophic muscles of young mdx mice show a latent myogenic phenotype that is implemented by the exposure to HDACi. Co-culture assays in vitro and co-transplantation experiments in vivo demonstrate that HDACi also improve Sca1-positive muscle interstitial cell ability to enhance the differentiation potential of adjacent satellite cells. Importantly, HDACi-induced myogenic phenotype and pro-regeneration activity were not observed in Sca1-positive muscle interstitial cells isolated from muscles of old mdx mice. The different phenotype of Sca1-positive muscle interstitial cells from mdx mice at different stages of disease progression correlated with the stage-dependent beneficial effect of HDACi, which were effective only at early stages of disease. Transplantation of Sca1-positive muscle interstitial cells isolated from regenerating young muscles into muscles of old mdx mice restored HDACi ability to increase myofiber size. These results indicate that Sca1-positive muscle interstitial cells are key cellular determinants of disease progression and mediate the beneficial effect of HDACi in a mouse model of muscular dystrophy. Isolation of Sca1+ muscle interstitial cells from TSA treated DMD/MDX mice and MuSc from DMD/MDX mice

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Activation of IFN1 signaling by TAK-981 in blood, spleen, or tumor of A20-tumor bearing or B16F10-tumor bearing mice

Project description:Intravenous administration of TAK-981 to Balb/c or C57BL/6 mice bearing A20 or B16F10 syngeneic tumors, respectively, resulted in a strong induction of IFN1 pathway genes in peripheral blood leukocytes, spleen and A20 tumor tissues. TAK- 981 dependent upregulation of IFN1 mRNA signature was determined from RNA-Seq data in peripheral blood, spleen and tumor of BALB/c mice bearing A20 tumors. Upregulation of IFN1 ssGSEA scores were calculated in peripheral blood at 4h (P = 0.0011) and 8h (P = 0.0001), in spleen at 4h (P = 0.0002) and 8h (P = 0.0020), and in tumor at 4h (P = 0.0095) and 8h (P = 0.0033) after treatment with the indicated doses of TAK-981. Dose dependent upregulation of IFN1 mRNA signature by TAK-981 was determined from RNA-Seq data in peripheral blood and spleen of C57BL/6 mice bearing B16F10 tumors. Upregulation of IFN1 ssGSEA scores in the blood at 4h (P = 0.001) and 8h (P = 0.0125) and in the spleen at 4h (P = 0.0019) and 8h (P = 0.0796) after treatment with the indicated concentrations of TAK-981. No upregulation of ssGSEA scores was detected in tumors at 4h (P=0.4295) or 8h (P=0.9706) after treatment with TAK-981. P values were calculated by Welch’s ANOVA test.

2021-04-23 | GSE173114 | GEO

CD169 is a marker of IFN-γ-stimulated inflammatory macrophages in brain tumor [WG vs TG]

Project description:Therapies against glioblastoma multiforme (GBM) have been largely ineffective due to the infiltration of immunosuppressive tumor-associated macrophages (TAMs). Recent studies demonstrated that TAMs can also be immune-activating. However, markers differentiating these heterogeneous macrophage populations have not been established. In this study, we identified a subset of macrophages expressing CD169 that promote an anti-tumoral microenvironment in GBM. Using single-cell transcriptome analysis, we found that CD169+ macrophages in human and mouse gliomas produced proinflammatory chemokines, leading to the accumulation of T cells and NK cells. Depletion of CD169+ macrophages shortened the survival of mice with gliomas and reduced the function of antitumor lymphocytes. We show that IFN-γ produced by NK cells was critical for the accumulation of CD169+ macrophages into gliomas. Additionally, CD169 expression on macrophages increased the phagocytosis of apoptotic glioma cells. Our finding suggests that the CD169+ subset of TAMs promotes antitumor immune responses against GBM.

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Expression data from regenerating mouse TA muscle

Project description:Mutations in fukutin-related protein (FKRP) gene are characterized with a lack of functionally glycosylated α-dystroglycan (F-α-DG). Surprisingly a small number of muscle fibers express strong F-α-DG. Here we investigate restoration of F-α-DG in FKRP mutant muscle and showed that the restoration of glycosylation is associated with muscle regeneration and dependent of the expression of both LARGE and partially functional FKRP. F-α-DG in regenerating fibers reaches normal levels and lasts for more than 4 weeks, however, no up-regulation of the LARGE and FKRP is detected during the regeneration process. These results suggest that FKRP P448L mutation clinically associated with severe CMD retains at least partial functions. Identification of factor(s) other than LARGE and FKRP could create new approaches for restoration of F-α-DG in mature muscle fibers with defects in FKRP function. We employed microarrays to detail changes in gene expression associated with muscle regeneration in wild-type and FKRP mutant skeletal muscle, and have identified a group of genes with altered expression between these mice during this regeneration process.

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