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 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
Project description:The inability of the beta-cell to meet the demand for insulin brought about by insulin resistance leads to type 2 diabetes. In adults, beta-cell replication is one of the mechanisms thought to cause the expansion of beta-cell mass. Efforts to treat diabetes require knowledge of the pathways that drive facultative beta-cell proliferation in vivo. A robust physiological stimulus of beta-cell expansion is pregnancy, and identifying the mechanisms underlying this stimulus may provide therapeutic leads for the treatment of type 2 diabetes. The peak in beta-cell proliferation during pregnancy occurs on day 14.5 of gestation in mice. Using advanced genomic approaches, we globally characterize the gene expression signature of pancreatic islets on day 14.5 of gestation during pregnancy. We identify a total of 1,907 genes as differentially expressed in the islet during pregnancy. We demonstrate that the islet's ability to compensate for relative insulin deficiency during metabolic stress is associated with the induction of both proliferative and survival pathways. A comparison of the genes induced in three different models of islet expansion suggests that diverse mechanisms can be recruited to expand islet mass. The identification of many novel genes involved in islet expansion during pregnancy provides an important resource for diabetes researchers to further investigate how these factors contribute to the maintenance of not only islet mass, but ultimately beta-cell mass.
2010-06-26 | E-MTAB-120 | biostudies-arrayexpress
Project description:comparison of mRNA expression in the islets of 3- and 12-month 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 | GSE72464 | GEO