Mus musculus strain:C57BL/6
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ABSTRACT:
PROVIDER: PRJNA252758 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:The epidemiological association of coxsackievirus B infection with type 1 diabetes suggests that therapeutic strategies that reduce viral load could delay or prevent disease onset. Moreover, recent studies suggest that treatment with antiviral agents against coxsackievirus B may help preserve insulin levels in type 1 diabetic patients. In the current study, we performed small RNA-sequencing to show that infection of immortalized trophoblast cells with coxsackievirus caused differential regulation of several miRNAs. One of these, hsa-miR-AMC1, was similarly upregulated in human pancreatic β cells infected with coxsackievirus B4. Moreover, treatment of β cells with non-cytotoxic concentrations of an antagomir that targets hsa-miR-AMC1 led to decreased CVB4 infection, suggesting a positive feedback loop wherein this microRNA further promotes viral infection. Interestingly, some predicted target genes of hsa-miR-AMC1 are shared with hsa-miR-184, a microRNA that is known to suppress genes that regulate insulin production in pancreatic β cells. Consistently, treatment of coxsackievirus B4-infected β cells with the hsa-miR-AMC1 antagomir was associated with a trend toward increased insulin production. Taken together, our findings implicate novel hsa-miR-AMC1 as a potential early biomarker of coxsackievirus B4-induced type 1 diabetes and suggest that inhibiting hsa-miR-AMC1 may provide therapeutic benefit to type 1 diabetes patients. Our findings also support the use of trophoblast cells as a model for identifying microRNAs that might be useful diagnostic markers or therapeutic targets for coxsackievirus B-induced type 1 diabetes.
2024-10-06 | GSE278756 | 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 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: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:Type 2 diabetes mellitus (DM) is characterized by insulin resistance and pancreatic beta-cell dysfunction. In high-risk subjects, the earliest detectable abnormality is insulin resistance in skeletal muscle. Impaired insulin-mediated signaling, gene expression, and glycogen synthesis, and accumulation of intramyocellular triglycerides have all been linked with insulin resistance, but no specific defect responsible for insulin resistance and DM has been identified in humans. To identify genes potentially important in the pathogenesis of DM, we analyzed gene expression in skeletal muscle from healthy metabolically characterized nondiabetic (family history negative and positive for DM) and diabetic Mexican-American subjects. We demonstrate that insulin resistance and DM associate with reduced expression of multiple nuclear respiratory factor-1 (NRF-1)-dependent genes encoding key enzymes in oxidative metabolism and mitochondrial function. While NRF-1 expression is decreased only in diabetic subjects, expression of both PPARg coactivator 1-alpha and -beta (PGC1-a/PPARGC1, and PGC1-b/PERC), coactivators of NRF-1 and PPARg-dependent transcription, is decreased in both diabetic subjects and family history positive nondiabetic subjects. Decreased PGC1 expression may be responsible for decreased expression of NRFdependent genes, leading to the metabolic disturbances characteristic of insulin resistance and DM. Human muscle samples were obtained from five subjects with type 2 diabetes and ten subjects without diabetes, as well as 5 aliquots from a single subject without diabetes. The subjects without diabetes were further classified as family history positive (four subjects) or family history negative (six subjects).
2010-04-27 | E-GEOD-21340 | biostudies-arrayexpress