E-MTAB-5264
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-5264 | ExpressionAtlas | 2020-07-10
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-5264-analysis-methods.tsv | Tabular | |||
| E-MTAB-5264-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-5264-configuration.xml | Xml | |||
| E-MTAB-5264-percentile-ranks.tsv | Tabular | |||
| E-MTAB-5264.condensed-sdrf.tsv | Tabular |
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Project description:Islets from 6-week old NOR and NOD mice were submitted to proteomics analysis to study differences in insulitis and type 1 diabetes development.
2024-05-21 | PXD021475 | Pride
Project description:scRNA-seq of Islets isolated from 8, 14 and 16 week NOD mice
2019-02-11 | GSE117770 | GEO
Project description:Type 1 diabetes (T1D) is an autoimmune disease triggered by T cell reactivity to protein antigens produced by the β-cells. Here we present a chronological compendium of transcriptional profiles from islets of Langerhans isolated from non-obese diabetic (NOD) mice ranging from 2 wks up to diabetes and compared to controls. Parallel analysis was made of cellular components of the islets. Myeloid cells populated the islets early during development in all mouse strains. This was followed by a type I interferon signature detectable at 4-6 wks of age only in diabetes susceptible mice. Concurrently, CD4 T cells were found within islets, many in contact with intra-islet antigen presenting cells. Early cellular signs of islet reactivity were detected by six wks. By 8 wks, NOD islets contained all major leukocytes populations and an inflammatory gene signature. This work establishes the natural transcriptional signature of T1D and provides a resource for future research. 57 RNA samples isolated from the pancreatic islets of langerhans of experimental mice: 2-18 wk old non-obese diabetic (NOD) and newly diabetic NOD were compared to controls: NOD.RAG-/-, B6.g7 and C57BL/6. There were 3 or 6 biological replicates per condition. All mice were female. All data was normalized using RMA in Arraystar. Data table includes normalized probe intensity for every probe.
2013-01-28 | E-GEOD-41203 | biostudies-arrayexpress
Project description:In the present work endothelial function in the aorta and femoral artery assessed in vivo by magnetic resonance imaging (MRI) was characterized in male and female 8-, 14-, 22-, 28-, and 40-week-old E3L.CETP and C57BL/6J mice. Vascular nitric oxide (NO), eicosanoids and hydrogen peroxide (H2O2) production in the aorta, were measured by electron paramagnetic resonance spectroscopy (EPR), mass spectrometry (LC/MS) and fluoresence assay, respectively. Endothelial-specific protein plasma biomarkers and global alterations in plasma proteome were asssesed by targeted and non-targeted preotomics, respectively. In C57BL/6J endothelial dysfunction was observed in 40-week-old female and male mice as evidenced by impaired endothelium-dependent vasodilation induced by acetylcholine (Ach) in the aorta or by flow in the femoral artery (flow-mediated vasodilation, FMD). In E3L.CETP mice age-dependent endothelial dysfunction was accelerated and appeared in 14-22-week-old male and 22-28-week-old female mice. In 40 week-old E3L.CETP mice endothelial dysfunction was severe in both male and female mice and was more pronounced as compared with age-matched C57BL/6J mice. Despite severe endothelial dysfunction in 40 week-old mice E3L.CETP mice neither in the aortic roots nor in brachiocephalic artery atherosclerotic plaques were not detected. Interestingly, in the presence of NOS-inhibitor (L-NAME), FMD was inhibited in all experimental groups. However, effect of L-NAME on Ach–induced vasodilation in E3L.CETP mice, was blunted as compared with C57BL/6J mice, in particular in young E3L.CETP female mice. Furthermore, Ach–induced vasodilation in the aorta was inhibited by catalase, while H2O2 production was increased, in young female but not in male E3L.CETP mice. A switch from NO to H2O2-dependent vasodilation in young female E3L.CETP mice was associated with a blunted systemic inflammation and lower number of differentially expressed proteins (DEPs) in plasma than in young E3L.CETP male mice as compared with age-and sex-matched C57BL/6J mice. However, female and male 40-week-old E3L.CETP mice displayed similar number of DEPs in plasma vs respective sex-matched younger E3L.CETP mice. In the present work endothelial function in the aorta and femoral artery assessed in vivo by magnetic resonance imaging (MRI) was characterized in male and female 8-, 14-, 22-, 28-, and 40-week-old E3L.CETP and C57BL/6J mice. Vascular nitric oxide (NO), eicosanoids and hydrogen peroxide (H2O2) production in the aorta, were measured by electron paramagnetic resonance spectroscopy (EPR), mass spectrometry (LC/MS) and fluoresence assay, respectively. Endothelial-specific protein plasma biomarkers and global alterations in plasma proteome were asssesed by targeted and non-targeted preotomics, respectively. In C57BL/6J endothelial dysfunction was observed in 40-week-old female and male mice as evidenced by impaired endothelium-dependent vasodilation induced by acetylcholine (Ach) in the aorta or by flow in the femoral artery (flow-mediated vasodilation, FMD). In E3L.CETP mice age-dependent endothelial dysfunction was accelerated and appeared in 14-22-week-old male and 22-28-week-old female mice. In 40 week-old E3L.CETP mice endothelial dysfunction was severe in both male and female mice and was more pronounced as compared with age-matched C57BL/6J mice. Despite severe endothelial dysfunction in 40 week-old mice E3L.CETP mice neither in the aortic roots nor in brachiocephalic artery atherosclerotic plaques were not detected. Interestingly, in the presence of NOS-inhibitor (L-NAME), FMD was inhibited in all experimental groups. However, effect of L-NAME on Ach–induced vasodilation in E3L.CETP mice, was blunted as compared with C57BL/6J mice, in particular in young E3L.CETP female mice. Furthermore, Ach–induced vasodilation in the aorta was inhibited by catalase, while H2O2 production was increased, in young female but not in male E3L.CETP mice. A switch from NO to H2O2-dependent vasodilation in young female E3L.CETP mice was associated with a blunted systemic inflammation and lower number of differentially expressed proteins (DEPs) in plasma than in young E3L.CETP male mice as compared with age-and sex-matched C57BL/6J mice. However, female and male 40-week-old E3L.CETP mice displayed similar number of DEPs in plasma vs respective sex-matched younger E3L.CETP mice.
2025-06-30 | PXD029562 | Pride
Project description:Abstract Two major dendritic cell (DC) subsets have been described in the islets of mice: The immunogenic CD8α-CD11b+ DCs and the tolerogenic CD8α+CD103+ DCs. We have recently reported on reduced numbers of the minor population of tolerogenic CD8α+CD103+ DCs in the pancreas of 5 week old pre-diabetic non-obese diabetic (NOD) mice. Aim: To analyze also the larger subset of CD11c+CD8α- DCs isolated from the pancreas of pre-diabetic NOD mice 1) for maturation and tolerance inducing molecules found abnormally expressed on CD8α+CD103+ DCs, and 2) for genome-wide gene expression to further elucidate abnormalities in underlying gene expression networks. Methods: CD11c+CD8α- DCs were isolated from 5 week old C57BL/6 and NOD pancreas. Expression of cell surface markers including CD86, CCR5, CD11b, CD103, Clec9a, CD24 and CD200R3 were measured by FACS. Genome-wide gene expression by microarray was assessed during the steady state and after in vitro LPS stimulation. Results: The steady state pancreatic CD11c+ CD8α- DCs during the pre-diabetic stage showed: 1) A reduced expression of several gene networks important for the prime functions of the cell, such as for cell renewal, immune stimulation and immune tolerance induction, for migration and for the provision of growth factors for beta cell regeneration. This general deficiency state was corroborated by a reduced in vivo proliferation (BrdU incorporation) of the cells and the reduced expression in FACS analysis of CD86, CCR5, CD103, Clec9a, CD24 and CD200R3 on the cells. 2) A hyper reactivity of these cells to LPS correlated with an enhanced pro-inflammatory state characterized by altered expression of a number of classical pro-inflammatory factors and cytokines. Conclusion: The NOD CD11c+CD8α- DCs seem to be Janus-faced depending on the conditions: Deficient in steady state with reduced immune stimulation capabilities also for tolerance induction; over-inflammatory with a molecular profile suggesting a preferential stimulatory capacity for Th1 cells when encountering a Pathogen-Associated Molecular Pattern (PAMP) in the form of LPS. We used microarray gene expression analysis to explain the abnormal expression of several cell surface markers involved in tolerace, migration and maturation in the steady-state and to measure the effect of a PAMP such as LPS We isolated RNA from FACS sorted CD11c+CD8α- DCs in 10 pooled pancreases from pre-diabetic NOD and non-diabetic C57BL/6 mice at 5 weeks. In addition, we treated in another experiment the isolated pancreas DCs with LPS (and PBS), incubated for 18h and measured gene expression. We compared gene expression between strains NOD vs C57BL/6 under steady-state and after in-vitro LPS/PBS stimulation.
2014-07-01 | E-GEOD-45028 | biostudies-arrayexpress
Project description:Gene expression in the islets of 10 day old, 4 week old and 12 week old Non-Obese Diabetic (NOD) mice vs. healthy, age-matched NOD.B10 control mice
| PRJNA627352 | ENA
Project description:Abstract Two major dendritic cell (DC) subsets have been described in the islets of mice: The immunogenic CD8α-CD11b+ DCs and the tolerogenic CD8α+CD103+ DCs. We have recently reported on reduced numbers of the minor population of tolerogenic CD8α+CD103+ DCs in the pancreas of 5 week old pre-diabetic non-obese diabetic (NOD) mice. Aim: To analyze also the larger subset of CD11c+CD8α- DCs isolated from the pancreas of pre-diabetic NOD mice 1) for maturation and tolerance inducing molecules found abnormally expressed on CD8α+CD103+ DCs, and 2) for genome-wide gene expression to further elucidate abnormalities in underlying gene expression networks. Methods: CD11c+CD8α- DCs were isolated from 5 week old C57BL/6 and NOD pancreas. Expression of cell surface markers including CD86, CCR5, CD11b, CD103, Clec9a, CD24 and CD200R3 were measured by FACS. Genome-wide gene expression by microarray was assessed during the steady state and after in vitro LPS stimulation. Results: The steady state pancreatic CD11c+ CD8α- DCs during the pre-diabetic stage showed: 1) A reduced expression of several gene networks important for the prime functions of the cell, such as for cell renewal, immune stimulation and immune tolerance induction, for migration and for the provision of growth factors for beta cell regeneration. This general deficiency state was corroborated by a reduced in vivo proliferation (BrdU incorporation) of the cells and the reduced expression in FACS analysis of CD86, CCR5, CD103, Clec9a, CD24 and CD200R3 on the cells. 2) A hyper reactivity of these cells to LPS correlated with an enhanced pro-inflammatory state characterized by altered expression of a number of classical pro-inflammatory factors and cytokines. Conclusion: The NOD CD11c+CD8α- DCs seem to be Janus-faced depending on the conditions: Deficient in steady state with reduced immune stimulation capabilities also for tolerance induction; over-inflammatory with a molecular profile suggesting a preferential stimulatory capacity for Th1 cells when encountering a Pathogen-Associated Molecular Pattern (PAMP) in the form of LPS. We used microarray gene expression analysis to explain the abnormal expression of several cell surface markers involved in tolerace, migration and maturation in the steady-state and to measure the effect of a PAMP such as LPS
2014-07-01 | GSE45028 | GEO
Project description:Tumors induce tolerance towards their antigens by producing the chemokine CCL21, leading to the formation of tertiary lymphoid organs (TLOs). Ins2-CCL21 transgenic, non-obese diabetic (NOD) mice express CCL21 in pancreatic β-cells and do not develop autoimmune diabetes. We investigated by which mechanisms CCL21 expression prevented diabetes. Islet infiltrates of 4 week-old Ins2-CCL21 mice were enriched in naïve CD4+ T cells and compartmentalized within networks of CD45- gp38+ CD31- fibroblastic reticular cell (FRC)-like stromal cells. Importantly, 12 week-old Ins2-CCL21 NOD islets contained FRC-like cells with enhanced expression of β-cell autoantigens and gene expression profiles consistent with regulatory, anti-inflammatory properties and increased contractility. Consistently, transgenic mice harbored fewer autoreactive T cells and higher proportion of Tregs in the islets. Using adoptive transfer and islet transplantation models, we demonstrate that the formation of TLOs in Ins2-CCL21 transgenic islets is critical for regulation of autoimmunity and while the effect is systemic, the induction may be mediated locally by lymphocyte trafficking through TLOs. Overall, our findings suggest that CCL21 promotes TLOs that differ from inflammatory TLOs associated with islets in T1D in that they resemble lymph nodes, contain FRC-like cells expressing β-cell autoantigens and are able to induce systemic and antigen-specific tolerance leading to diabetes prevention. These findings suggest that CCL21 may be exploited for novel immunoregulation approaches to treat autoimmune diabetes.
2019-09-23 | GSE130979 | GEO
Project description:Mouse platelets were collected following 4 days of exercise or standard-housing from 8-week-old C57BL/6J mice and mass spectrometry performed (5 mice per group). The analysis revealed differences in the proteomic content of platelets isolated from standard-housed and exercising mice.
2023-08-18 | PXD041700 | Pride
Project description:Six to eight week old female C57BL/6J mice were exposed to 2 Gy of whole body γ radiation and mammary glands were surgically removed 2-month after radiation. RNA was isolated and microarray hybridization performed for gene expression analysis.
2014-05-01 | GSE57196 | GEO