Ontology highlight
ABSTRACT:
PROVIDER: PRJNA252781 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes
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Project description:The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (islet)
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Project description:The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (Min6 cells)
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Project description:comparison of microRNA expression in the islets of 3- and 12-months old male Wistar rats Aging is a risk factor for a majority of metabolic diseases including type 2 diabetes. During aging pancreatic beta-cell function decreases leading to impaired insulin secretion and proliferation and to an increase in apoptosis. Impairment of pancreatic beta cell functions and survival has been linked to gene expression changes. The aim of our study was to obtain a global expression profile of microRNAs and mRNAs of pancreatic islets of 3 and 12 month old male Wistar rats in order to identify the changes occurring during aging.
2015-09-30 | GSE72465 | GEO
Project description:β-cells are a type of endocrine cell found in pancreatic islets that synthesize, store and release insulin. Destruction of these cells in type 1 diabetes leads to a lifelong dependence on exogenous insulin administration for survival. Here we employ RNA-seq to examine the promotion of β-like cell regeneration with EZH2 inhibition in pancreatic ductal epithelial cells and exocrine cells isolated from type 1 diabetic donor tissue.
2024-01-10 | GSE247275 | GEO
Project description:Type 2 diabetes (T2D) is a complex chronic disease that results from pancreatic β-cell dysfunction and insulin resistance. Human genetic evidence supports a pivotal role of HNF1A, encoding hepatocyte nuclear factor 1A, in the pathophysiology of mendelian and type 2 diabetes. Recent single-cell genomic studies also reveal HNF1A as a key transcription factor underlying β-cell heterogeneity and disease progression. We now demonstrate that HNF1A-deficient diabetes is caused by β-cell-autonomous defects, and show that HNF1A governs not only β-cell transcription, but also a broad RNA splicing program. We uncover a regulatory hierarchy in which HNF1A controls transcription of A1CF, which in turn regulates splicing of genes important for membrane transport, lysosome, and secretory functions. Genetic variants that increase human pancreatic islet A1CF expression are associated with improved glycemia, increased insulin secretion, and decreased T2D susceptibility. Furthermore, β-cells from T2D individuals exhibit a profound disruption of A1CF-dependent splicing. These findings link HNF1A-deficiency to a β-cell RNA splicing defect that is impaired in Mendelian diabetes and T2D.
2025-08-03 | GSE277551 | GEO
Project description:Type 2 diabetes (T2D) is a complex chronic disease that results from pancreatic β-cell dysfunction and insulin resistance. Human genetic evidence supports a pivotal role of HNF1A, encoding hepatocyte nuclear factor 1A, in the pathophysiology of mendelian and type 2 diabetes. Recent single-cell genomic studies also reveal HNF1A as a key transcription factor underlying β-cell heterogeneity and disease progression. We now demonstrate that HNF1A-deficient diabetes is caused by β-cell-autonomous defects, and show that HNF1A governs not only β-cell transcription, but also a broad RNA splicing program. We uncover a regulatory hierarchy in which HNF1A controls transcription of A1CF, which in turn regulates splicing of genes important for membrane transport, lysosome, and secretory functions. Genetic variants that increase human pancreatic islet A1CF expression are associated with improved glycemia, increased insulin secretion, and decreased T2D susceptibility. Furthermore, β-cells from T2D individuals exhibit a profound disruption of A1CF-dependent splicing. These findings link HNF1A-deficiency to a β-cell RNA splicing defect that is impaired in Mendelian diabetes and T2D.
2025-08-03 | GSE277552 | GEO
Project description:Type 1 diabetes risk genes mediate pancreatic beta cell survival in response to proinflammatory cytokines
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Project description:Pancreatic islet beta cell heterogeneity has been identified, which plays a pivotal role in the pathological alterations of pancreatic islets in type 2 diabetes (T2D) mice. However, pathological alterations of beta cells in type 2 diabetes (T2D) mice remain to be investigated. We isolated pancreatic islets from the control and T2D mice and conducted scRNA-seq analysis using the 10x Genomics platform. Pathological alterations of beta cells in T2D were also explored.
2022-04-09 | GSE200531 | GEO
Project description:Transcriptional and posttranscriptional regulatory networks play a crucial role in the maintenance and adaptation of pancreatic beta-cell function. In this study we show that the levels of the prototypic neuroendocrine miRNA-7 are regulated in islets of obese, diabetic and aged mouse models. Using gain- and loss-of-function models we demonstrate that miR-7 regulates crucial members of the endocrine pancreatic transcriptional network controlling differentiation and insulin synthesis. Importantly, it also directly regulates key proteins in the insulin granule secretory machinery. These results reveal an interconnecting miR-7 genomic circuit that influences beta-cell differentiation, insulin synthesis and release and define a role for miR-7 as an endocrine checkpoint to stabilize beta-cell function during metabolic stress. These findings have implications for miR-7 inhibitors as potential therapies for type 2 diabetes and neurodegenerative diseases. Either miR-7a2 or miR-7b were over-expressed in MIN6 cells using an adenoviral vector. The miR-7a infection was performed in duplicates. In addition, a GFP over-expression in MIN6 using the same viral vector served as control. We also explored the consequence of miR-7a2 deletion in pancreatic beta-cells by generating a beta-cells specific miR-7a2 knock-out using the Lox/Cre system in a C57BL/6 background. We profiled gene expression in mutant and wild-type (control) islets.
2015-06-30 | E-GEOD-48195 | biostudies-arrayexpress