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PROVIDER: PRJEB59117 | ENA |
REPOSITORIES: ENA
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Project description:Identification of novel and already known altered micoRNAs lead to a deeper understanding of the development of type 1 diabetes mellitus
| PRJEB59759 | ENA
Project description:Pancreatic β-cells are responsible for production and secretion of insulin in response to increasing blood glucose levels. Therefore, defects in pancreatic β-cell function lead to hyperglycemia and diabetes mellitus. Understanding the molecular mechanisms governing β cell function is crucial for development of novel treatment strategies for this disease. The aim of this project was to investigate the role of Cnot3, part of CCR4-NOT complex, major deadenylase complex in mammals, in pancreatic β cell function. Cnot3βKO islets display decreased expression of key regulators of β cell maturation and function. Moreover, they show an increase of progenitor cell markers, β cell-disallowed genes and genes relevant to altered β cell function. Cnot3βKO islets exhibit altered deadenylation and increased mRNA stability, partly accounting for the increase of those genes. Together, these data reveal that CNOT3-mediated mRNA deadenylation and decay constitute previously unsuspected post-transcriptional mechanisms essential for β cell identity.
2020-08-31 | PXD018403 | Pride
Project description:To understand organ (dys)function it is important to have a complete inventory of its cell types and the corresponding markers that unambiguously identify these cell types. This is a challenging task, in particular in human tissues, because unique cell-type markers are typically unavailable, necessitating the analysis of complex cell type mixtures. Transcriptome-wide studies on pancreatic tissue are typically done on pooled islet material. To overcome this challenge we sequenced the transcriptome of thousands of single pancreatic cells from deceased organ donors with and without type 2 diabetes (T2D) allowing in silico purification of the different cell types. We identified the major pancreatic cell types resulting in the identification of many new cell-type specific and T2D-specific markers. Additionally we observed several subpopulations within the canonical pancreatic cell types, which we validated in situ. This resource will be useful for developing a deeper understanding of pancreatic biology and diabetes mellitus. Human cadaveric pancreata were used to extract islets of Langerhans, which were kept in culture until single-cell dispersion and FACS sorting. Single-cell transcriptomics was performed on live cells from this mixture using CEL-seq or on cells stained for CD63, CD13, TGFBR3 or CD24 and CD44. The RaceID algorithm was used to identify clusters of cells corresponding to the major pancreatic cell types and to mine for novel cell type-specific genes as well as subpopulations within the known pancreatic cell types.
2016-06-24 | E-GEOD-81076 | biostudies-arrayexpress
Project description:Understanding the role of Type 1 diabetes mellitus in osteoarthritis
| PRJNA817158 | ENA
Project description:Evidence suggests that diabetes mellitus is a promoting factor of sarcopenia; mechanism of how diabetes mellitus accelerates the development of sarcopenia is not known. We have recently established a model of diabetes-induced skeletal muscle mass loss in mice by using streptozotocin. We used microarrays to detail the global programme of gene expression underlying skeletal muscle atrophy in STZ treated mice and identified up-regulated or down-regulated genes during this process.
2018-12-11 | GSE123540 | GEO
Project description:Alterations of oral microbiota and impact on the gut microbiome in type 1 diabetes mellitus revealed by multi-omic analysis
| PRJEB50825 | ENA
Project description:Alterations in the expression of key transcription factors can be harmful for pancreatic beta cell homeostasis and could lead to diabetes. This study uncovered that Prox1 overexpression obstructs beta cell maturation and results in severe hyperglycemia. The function of β-cells is key for glucose homeostasis because they supply insulin to the entire body. Genetic or metabolic conditions that disrupt the complex physiology of β-cells can lead to diabetes mellitus, a prevalent life-threatening disease. Here we investigated whether sustained Prox1 expression is incompatible with β-cell development using a transgenic mouse approach, and report that β-cell maturation is drastically impaired in the presence of high levels of Prox1. We used microarrays to identify gene expression profiles and pathways that are differentially activated when Prox1 is overexpressed in murine pancreatic beta cells.
2016-02-11 | E-GEOD-68133 | biostudies-arrayexpress
Project description:Type 2 diabetes mellitus represents a major health problem with increasing prevalence worldwide. Limited efficacy of current therapies have prompted a search for novel therapeutic options. Here we show that treatment of pre-diabetic mice with mitochondrially targeted tamoxifen, a potential anti-cancer agent with senolytic activity, improves glucose tolerance and reduces body weight with most pronounced reduction of visceral adipose tissue due to reduced food intake, suppressed adipogenesis and elimination of senescent cells. Glucose-lowering effect of mitochondrially targeted tamoxifen is linked to improvement of type 2 diabetes mellitus-related hormones profile and is accompanied by reduced lipid accumulation in liver. Lower senescent cell burden in various tissues, as well as its inhibitory effect on pre-adipocyte differentiation, results in lower level of circulating inflammatory mediators that typically enhance metabolic dysfunction. Targeting senescence with mitochodrially targeted tamoxifen thus represents an approach to the treatment of type 2 diabetes mellitus and its related comorbidities, promising a complex impact on senescence-related pathologies in aging population of patients with type 2 diabetes mellitus with potential translation into the clinic.
2022-05-20 | PXD031710 | Pride
Project description:More and more studies pointed out that BM was the primary target of diabetes mellitus-induced damage. The aim of this study was to determine whether distinct gene expression profiles are associated with altered functions of bone marrow cells in diabetes mellitus type 2 mice. We performed global gene expression analysis in the bone marrow cells of 3 diabetic mice and 3 non-diabetic mice using Affymetrix Gene Chip Mouse Gene 1.0 ST Arrays. The gene expression patterns of diabetic mice were compared with those of nondiabetic ones using fold change. Validity of microarray results was examined by quantitative RT-PCR.
2015-05-07 | GSE68619 | GEO
Project description:The majority of congenital heart disease cases lack a definitive cause, suggesting the role of gene-environment interactions (GxE) in disease pathogenesis. Maternal diabetes mellitus (matDM) is among the most prevalent environmental risk factors for CHD and matDM associated oxidative stress is known to disrupt cardiac development. Here, we demonstrate that NOTCH1 haploinsufficient endothelial cells have an altered transcriptomic response to oxidative stress compared to control endothelial cells, with an exacerbated effect on gene regulatory networks crucial for endocardial cushion morphogenesis.
2024-10-18 | GSE279323 | GEO