Senescence is a cellular phenotype present in health and disease, characterized by a stable cell cycle arrest and an inflammatory response, denominated senescence-associated secretory phenotype (SASP). The SASP is important in influencing the behaviour of neighbouring cells and altering the microenvironment; yet, this role has been mainly attributed to soluble factors. Here, we show that both the soluble factors in addition to small extracellular vesicles (sEV) are capable of transmitting paracrine senescence to nearby cells. Analysis of individual cells internalizing sEV, using a Cre-reporter system, show a positive correlation between sEV uptake and senescence activation. Interestingly, we find an increase in the number of multivesicular bodies during senescence in vivo. sEV protein characterization by mass spectrometry (MS) followed by a functional siRNA screen identify the Interferon Induced Transmembrane Protein 3 (IFITM3) as partially responsible for transmitting senescence to normal cells. Altogether, we found that sEV contribute to paracrine senescence. Overall design: SASP related mRNA transcripts in HFFF2 treated with sEV from iRAS cells in comparison with HFFF2 treated with sEV from iC cells
Small Extracellular Vesicles Are Key Regulators of Non-cell Autonomous Intercellular Communication in Senescence via the Interferon Protein IFITM3.
Disease, Subject
View SamplesA comparative analysis of gene expression of 3 different experiments; 1. Perinate or adult-tagged GFP+YFP+ and bulk GFP+YFP- Tregs, 2. FL or BM-derived Tregs 3. Perinate or adult thymic Tregs.
Immune tolerance. Regulatory T cells generated early in life play a distinct role in maintaining self-tolerance.
Sex, Age, Specimen part
View SamplesA comparative analysis of gene expression of perinate or adult Aire-GFP+ and GFP- MECs in WT or Aire-KO thymus
Immune tolerance. Regulatory T cells generated early in life play a distinct role in maintaining self-tolerance.
Sex, Age, Specimen part
View SamplesComparison of gene expression level of 3T3-L1, PMEF and ES cell derived adipocytes to eWAT samples.
Highly efficient differentiation of embryonic stem cells into adipocytes by ascorbic acid.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment, Time
View SamplesA phenotypically and functionally distinct population of CD4+ Foxp3+ T cells (Tregs) rapidly accumulates in acutely injured skeletal muscle of mice, just as invading myeloid-lineage cells switch from a pro-inflammatory to a pro-regenerative state. Analysis of gene expression of Tregs and CD4+Foxp3- T cells (Tconvs) from injured muscle and spleen revealed that the transcriptome of muscle Treg cells is distinct from that of splenic Tregs. A set of genes is uniquely expressed by muscle Tregs, while another set is over-expressed by the two muscle populations vis--vis their two spleen counterparts.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment, Time
View SamplesA comparative analysis of gene expression of injured skeletal muscle from wild-type (Foxp3-DTR-) and Treg-depleted (Foxp3-DTR+) mice showed that Treg cells are critical for effective repair and regeneration of acute injury of skeletal muscle.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment, Time
View SamplesGlobal gene expression analysis of injured skeletal muscle showed that amphiregulin (Areg), a growth factor over-expressed by muscle Treg cells, enhances muscle regeneration both in the presence and in the absence of Tregs.
A special population of regulatory T cells potentiates muscle repair.
Age, Specimen part, Treatment, Time
View SamplesCD4+Foxp3+ regulatory T cells (Tregs) accumulate in skeletal muscle from dystrophin-deficient mdx mice. Analysis of global gene expression in muscles from mdx mice treated with anti-CD25 compared with muscles from mdx mice treated with control antibody revealed that Tregs partially protect mdx mice from muscle pathology and promote muscle repair/regeneration.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment
View SamplesMice with homozygous null mutations in the HDL receptor (SR-BI) and apoE genes (SR-BI KO/apoE double KO (dKO) mice) spontaneously develop occlusive, atherosclerotic coronary artery disease (CAD) and die prematurely (50% mortality at 42 days of age) on standard chow diet feeding. Microarray analysis was performed to investigate the changes in gene expression profiles during the development of spontaneous severe CAD, which includes myocardial infarction and heart failure. These data will provide new insights in understanding the pathophysiology of CAD.
Identification of apolipoprotein D as a cardioprotective gene using a mouse model of lethal atherosclerotic coronary artery disease.
Age, Specimen part
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