Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-Cell RNAseq Reveals That Pancreatic β-Cells From Very Old Male Mice Have a Young Gene Signature

ABSTRACT: Aging improves pancreatic β-cell function in mice. This is a surprising finding since aging is typically associated with functional decline. We performed single-cell RNA sequencing of β-cells from 3 and 26 month old mice to explore how changes in gene expression contribute to improved function with age. The old mice were healthy, had reduced blood glucose levels and increased β-cell mass, which correlated to their body weight. β-cells from young and old mice had similar transcriptome profiles. In fact, only 193 genes (0.89% of all detected genes) were significantly regulated (≥ 2-fold; false discovery rate < 0.01; normalized counts > 5). Of these, 183 were downregulated and mainly associated with pathways regulating gene expression, cell cycle, cell death and survival as well as cellular movement, function and maintenance. Collectively, our data show that β-cells from very old mice have transcriptome profiles similar to those of young mice. These data support previous findings that aging is not associated with reduced β-cell mass or functional β-cell decline in mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE83146 | GEO | 2016/06/30

SECONDARY ACCESSION(S): PRJNA325131

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Single-Cell RNAseq Reveals That Pancreatic Î²-Cells From Very Old Male Mice Have a Young Gene Signature

Project description:Aging improves pancreatic Î²-cell function in mice. This is a surprising finding since aging is typically associated with functional decline. We performed single-cell RNA sequencing of Î²-cells from 3 and 26 month old mice to explore how changes in gene expression contribute to improved function with age. The old mice were healthy, had reduced blood glucose levels and increased Î²-cell mass, which correlated to their body weight. Î²-cells from young and old mice had similar transcriptome profiles. In fact, only 193 genes (0.89% of all detected genes) were significantly regulated (â¥ 2-fold; false discovery rate < 0.01; normalized counts > 5). Of these, 183 were downregulated and mainly associated with pathways regulating gene expression, cell cycle, cell death and survival as well as cellular movement, function and maintenance. Collectively, our data show that Î²-cells from very old mice have transcriptome profiles similar to those of young mice. These data support previous findings that aging is not associated with reduced Î²-cell mass or functional Î²-cell decline in mice. Single-cell RNA sequencing of mouse pancreatic islet beta cells

2016-06-30 | E-GEOD-83146 | biostudies-arrayexpress

Dataset on transcriptome signature of skeletal muscle of young, adult and aged mice

Project description:Skeletal muscle aging is characterized by a progressive decline in muscle mass and function, which is referred to as sarcopenia. However, the molecular mechanisms implicated in sarcopenia remain unclear. In this dataset, we include the expression data obtained from gastrocnemius muscle of young, mature adult and old C57BL6 male mice.

2021-08-18 | GSE136266 | GEO

Aging-dependent demethylation of regulatory elements correlates with chromatin state and improved insulin secretion by pancreatic ? cells

Project description:Aging at the cellular level is driven by changes in gene activity and epigenetic state that are only partially understood. We performed a comprehensive epigenomic analysis of the pancreatic ? cell, key player in glucose homeostasis and diabetes, in adolescent and very old mice. Globally, we observe a general methylation drift resulting in an overall more leveled methylome, suggesting that the maintenance of highly differential methylation patterns becomes compromised with advanced age. Importantly, we discover targeted changes in the methylation status of ? cell proliferation and function genes that go against the global methylation drift, are specific to ? cells, and correlate with repression of the proliferation program and activation of metabolic regulators. These targeted alterations frequently occur at distal cis-regulator elements, and are associated with specific chromatin marks and transcription factor occupancy in young ? cells. Strikingly, we find the insulin secretory response to glucose much improved in mature ? cells in mice, as predicted by the changes in methylome and transcriptome and in contrast to the decline in function observed in aged human ? cells. Thus, aging of terminally differentiated cells in mammals is not always coupled to functional decline. RNA-seq was done on 3 biological replicas from old and three from young beta cells. each sample originated from a pool of 5-10 mic.e H3K27me3 ChIP-seq was done with two replicas for old mice (pool of 4-7 mice) and the rest of the ChIPseq (H3K4me1, H3K27ac and young H3K27me3) was sone with one sample (pool of few mice). BIS-seq was done on one sample from a pool of 10 young mice and one sample of a pool of old mice (18-22 months old)

2015-09-01 | E-GEOD-68618 | biostudies-arrayexpress

Restoration of CPEB4 Prevents Muscle Stem Cell Senescence during Aging

Project description:Muscle stem cells (MuSCs) are required for muscle regeneration. In resting muscles, MuSCs are kept in quiescence. After injury, MuSCs undergo rapid activation, proliferation and differentiation to repair damaged muscles. Age-associated impairments in stem cell functions correlate with a decline in somatic tissue regeneration capacity during aging. However, the mechanisms underlying the molecular regulation of adult stem cell aging remain elusive. Here, we obtained quisecent MuSCs from young, old, geriatric mice for high resolution mass spectrometry Bruker timsTOF Pro. By comparison of young proteome to old MuSCs proteome or geriatric MuSC proteome, we identified the pathways that are differentially during aging.

2023-06-26 | PXD041614 | Pride

An atlas of the aging lung mapped by single cell transcriptomics and deep tissue proteomics

Project description:Aging promotes lung function decline and susceptibility to chronic lung diseases, which are the third leading cause of death worldwide. We used single cell transcriptomics and mass spectrometry to quantify changes in cellular activity states of 30 cell types and the tissue proteome from lungs of young and old mice. Aging led to increased transcriptional noise, indicating deregulated epigenetic control. We observed highly distinct effects of aging on cell type level, uncovering increased cholesterol biosynthesis in type-2 pneumocytes and lipofibroblasts as a novel hallmark of lung aging. Proteomic profiling revealed extracellular matrix remodeling in old mice, including increased collagen IV and XVI and decreased Fraser syndrome complex proteins and Collagen XIV. Computational integration of the aging proteome and single cell transcriptomes predicted the cellular source of regulated proteins and created a first unbiased reference of the aging lung. The lung aging atlas can be accessed via an interactive user-friendly webtool at: https://theislab.github.io/LungAgingAtlas

2019-01-21 | PXD012307 | Pride

Transcription profiling of long-term hematopoietic stem cells from old and young mice to investigate the mechanisms of hematopoietic aging

Project description:Loss of immune function and an increased incidence of myeloid leukemia are two of the most clinically significant consequences of aging of the hematopoietic system. To better understand the mechanisms underlying hematopoietic aging, we evaluated the cell intrinsic functional and molecular properties of highly purified long-term hematopoietic stem cells (LT-HSCs) from young and old mice. We found that LT-HSC aging was accompanied by cell autonomous changes, including increased stem cell self-renewal, differential capacity to generate committed myeloid and lymphoid progenitors, and diminished lymphoid potential. Expression profiling revealed that LT-HSC aging was accompanied by the systemic down-regulation of genes mediating lymphoid specification and function and up-regulation of genes involved in specifying myeloid fate and function. Moreover, LT-HSCs from old mice expressed elevated levels of many genes involved in leukemic transformation. These data support a model in which age-dependent alterations in gene expression at the stem cell level presage downstream developmental potential and thereby contribute to age-dependent immune decline, and perhaps also to the increased incidence of leukemia in the elderly. 3 old mice and 5 young mice were assayed

2007-12-19 | E-GEOD-4332 | biostudies-arrayexpress

Transcriptomic analysis to identify genes associated with hypothalamus vulnerability in aging mice with cognitive decline

Project description:Normal aging process is accompanied by cognitive decline. Studies have shown that the hypothalamus plays an important role in regulating aging and cognition. However, the exact molecular mechanism remains unclear. Therefore, the present study aimed to identify predictors of aging cognitive decline in the hypothalamus. The behavioral experiment was used to identify learning and memory differences between young and old mice. Transcriptome sequencing was performed on the hypothalamus of young and old mice to identify potential genes.Our data provide the related genes ,which may be potential predictors of cognitive function in the elderly population, which will establish an important foundation for us to further explore the molecular mechanism.

2024-07-01 | GSE240365 | GEO

Absolute Proteome Analysis of Hippocampus, Cortex and Cerebellum in Aged and Young Mice Reveals Changes in Energy Metabolism

Project description:Aging is associated with a general decline of cognitive functions, and it is widely accepted that this decline results from changes in expression of proteins involved in regulation of synaptic plasticity. However, several lines of evidence has accumulated that impaired function of aged brain may be related to significant alterations in the energy metabolism. In the current study, we employed the label-free „Total protein approach” (TPA) method to focus on similarities and differences in energy metabolism proteomes of young (1 month-old) and aged (22 month-old) murine brains. We quantified over 7,000 proteins in each of three analyzed brain structures: hippocampus, cerebral cortex and cerebellum. To the best of our knowledge, this is the most extensive quantitative proteomic description of energy metabolism pathways during physiological aging of mice. The analysis demonstrates that aging does not affect significantly the abundance of total proteins in the studied brain structures, however, the levels of proteins constituting energy metabolism pathways differ significantly between young and aged mice.

2022-02-17 | PXD025978 | Pride

Aging-dependent demethylation of regulatory elements correlates with chromatin state and improved insulin secretion by pancreatic β cells

Project description:Aging at the cellular level is driven by changes in gene activity and epigenetic state that are only partially understood. We performed a comprehensive epigenomic analysis of the pancreatic β cell, key player in glucose homeostasis and diabetes, in adolescent and very old mice. Globally, we observe a general methylation drift resulting in an overall more leveled methylome, suggesting that the maintenance of highly differential methylation patterns becomes compromised with advanced age. Importantly, we discover targeted changes in the methylation status of β cell proliferation and function genes that go against the global methylation drift, are specific to β cells, and correlate with repression of the proliferation program and activation of metabolic regulators. These targeted alterations frequently occur at distal cis-regulator elements, and are associated with specific chromatin marks and transcription factor occupancy in young β cells. Strikingly, we find the insulin secretory response to glucose much improved in mature β cells in mice, as predicted by the changes in methylome and transcriptome and in contrast to the decline in function observed in aged human β cells. Thus, aging of terminally differentiated cells in mammals is not always coupled to functional decline.

2015-09-01 | GSE68618 | GEO

Transcription profiling of hematopoietic stem cell aging

2005-08-16 | E-SMDB-3450 | biostudies-arrayexpress