Mus musculus strain:C57BL/6
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA252758 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (islet)
| PRJNA252783 | ENA
Project description:The microRNA-200 family regulates pancreatic beta-cell survival in type 2 diabetes (Min6 cells)
| PRJNA252782 | ENA
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: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
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
Project description:Type 1 diabetes risk genes mediate pancreatic beta cell survival in response to proinflammatory cytokines
| PRJNA847952 | ENA