Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A comprehensive analysis of microRNA alteration in ApoE(-/-) mice model of white adipose tissue injury induced by chronic intermittent hypoxia

ABSTRACT: In the current study, we first used miRNA-seq technology to identify the miRNA expression profile of CIH-induced WAT dysfunction in a mouse model. Then, Gene Ontology (GO) and KEGG analyses were utilized to analyze the differential expression of mRNA targeting function, followed by RT-qPCR validation. Finally, we constructed a regulatory network for miRNA–mRNA based on the above results. This study contributes to a more detailed description of the WAT dysfunction mechanism associated to OSA.

ORGANISM(S): Mus musculus

PROVIDER: GSE292464 | GEO | 2025/03/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Comprehensive analysis of differentially expressed miRNAs in mice with kidney injury induced by chronic intermittent hypoxia

Project description:In this study, the altered miRNA profiles in a chronic intermittent hypoxia (CIH) mouse model were investigated, aiming to provide novel clues for delineating the underlying mechanisms of OSA-induced kidney injury.

2022-10-20 | GSE202480 | GEO

Acetylome analyses provide new insights into the effect of chronic intermittent hypoxia on hypothalamus-dependent endocrine metabolism impairment

Project description:Background: Paediatric obstructive sleep apnoea (OSA) is a highly prevalent sleep disorder resulting in chronic intermittent hypoxia (CIH) that has been linked to metabolism and endocrine impairment. Protein acetylation, which is a frequently occurring posttranslational modification, plays pivotal roles in the regulation of hypothalamic processes. However, the effects of CIH-induced global protein acetylation on hypothalamic function and endocrine metabolism remain poorly understood. Methods: To bridge this knowledge gap, we conducted a study utilizing liquid chromatography–tandem mass spectrometry to analyse the lysine acetylome and proteome of the hypothalamus in healthy infantile mice exposed to 4 weeks of intermittent hypoxia (as a CIH model) compared to normoxic mice (as controls). Results: Our analysis identified and quantified 2699 lysine acetylation sites in 2453 proteins. These acetylated proteins exhibited disruptions primarily in endocrine metabolism, the citrate cycle (TCA cycle), synapse function, and circadian entrainment. Additionally, we observed significant downregulation of proteins that are known to be involved in endocrine hormone secretion. Metabolomic analysis of plasma suggested significant alterations in glycerophospholipid and amino acids metabolism, neuroactive ligand-receptor interaction and serotonergic synapse in children with OSA; these changes may represent potential mechanisms underlying the pathogenesis of OSA in children. Conclusion: This study aimed to elucidate the molecular mechanisms underlying CIH-induced alterations in protein acetylation within the hypothalamus. By providing valuable insights into the pathophysiological processes associated with CIH and their impacts on hypothalamic function, our findings contribute to a deeper understanding of the consequences stemming from CIH-induced changes in protein acetylation within the hypothalamus, as well as its potential role in endocrine impairment.

2024-10-17 | PXD051767 | Pride

Chronic intermittent hypoxia enhances pathological tau seeding, propagation, and accumulation, and exacerbates Alzheimer’s-like memory and synaptic plasticity deficits and molecular signatures

Project description:Obstructive sleep apnea (OSA), characterized by sleep fragmentation and chronic intermittenthypoxia (CIH), is a risk factor for Alzheimer’s disease (AD) progression. Recent epidemiologicalstudies point to CIH as the best predictor of developing cognitive decline and AD in elderly withOSA. However, the precise underlying mechanism(s) remain unknown. The present study wasundertaken to evaluate the effect of CIH on pathological human tau seeding, propagation, andaccumulation, cognition, synaptic plasticity, neuronal network excitability, and gene expressionprofiles in a P301S human mutant tau mouse model of AD and related tauopathies. We exposed 4-4.5-month-old, male, P301S and WT mice to an 8-week CIH protocol (6 min cycle:21% O 2 to 8% O 2 to 21% O 2 , 80 cycles per 8 h during daytime), and assessed its effect on taupathology and various AD-related phenotypic and molecular signatures. Age- and gender-matched P301S and WT mice were reared in normoxia (21% O 2 ) as experimental controls. CIH significantly enhanced pathological human tau seeding and spread across connected brain circuitry in P301S mice; it also increased phospho-tau load. CIH also exacerbated memory and synaptic plasticity deficits in P301S mice. However, CIH had no effect on seizure susceptibility and network hyperexcitability in these mice. Finally, CIH exacerbated AD-related pathogenic molecular signaling in P301S mice. CIH-induced increase in pathologic human tau seeding and spread and exacerbation of other AD- related impairments provide new insights into the role of CIH and OSA in AD pathogenesis.

2021-03-24 | GSE169478 | GEO

Gene expression and phenotypic characterization of mouse heart after chronic constant or intermittent hypoxia

Project description:Chronic constant hypoxia (CCH), such as in pulmonary diseases or high altitude, and chronic intermittent hypoxia (CIH), such as in sleep apnea, can lead to major changes in the heart. The molecular mechanisms underlying these cardiac alterations are not well understood. We hypothesized that analysis on the changes in gene expression could help to delineate such mechanisms. In addition, the differences that can be anticipated between CCH and CIH could be potentially dissected. Current study used CCH and CIH mouse models combined with cDNA microarrays to determine the changes of gene expression in CCH or CIH mice heart. Keywords = heart Keywords = hypoxia Keywords = mouse Keywords = microarray Keywords: time-course

2010-06-10 | E-GEOD-2271 | biostudies-arrayexpress

Expression data from mouse aorta with chronic intermittent hypoxia exposure

Project description:Atherosclerosis is the pathological basis of cardiovascular disease. Obstructive sleep apnea aggravates atherosclerosis, and chronic intermittent hypoxia (CIH) as a prominent feature of obstructive sleep apnea plays an important role during the process of atherosclerosis. The mechanisms of CIH in the development of atherosclerosis remain unclear. The microarray was used to investigate differentially expressed mRNAs and long noncoding RNAs (lncRNAs) in aorta from five groups of ApoE-/- mice fed with a high-fat diet and exposed to various conditions: normoxia for 8 weeks, CIH for 8 weeks, normoxia for 12 weeks, CIH for 12 weeks, or CIH for 8 weeks followed by normoxia for 4 weeks.

2020-02-14 | GSE145221 | GEO

In-depth Proteomics and Phosphoproteomics Reveal Biomarkers and Molecular Pathways of Chronic Intermittent Hypoxia in Mice

Project description:Obstructive sleep apnea (OSA) syndrome is characterized by Chronic Intermittent Hypoxia (CIH). In this study, we employed Data-independent acquisition (DIA) Mass Spectrometry to conduct comprehensive proteomic and phosphoproteomic profiling of a murine model subjected to Chronic Intermittent Hypoxia (CIH), a model we had previously established. Utilizing three CIH and three normal control genioglossus samples, we gathered valuable insights into the molecular alterations associated with CIH.

2024-07-08 | PXD053746 |

miRNA-Mediated Suppression of a Cardioprotective Cardiokine as a Novel Mechanism Exacerbating Post-MI Remodeling by Sleep Breathing Disorders [RNA-Seq]

Project description:This study provides the first evidence that MI+CIH upregulates miR-214-3p, suppresses cardiac CTRP9 expression, and exacerbates cardiac remodeling, suggesting that CTRP9 may be a novel therapeutic target against pathologic remodeling in MI patients with OSA

2019-09-25 | GSE138008 | GEO

miRNA-Mediated Suppression of a Cardioprotective Cardiokine as a Novel Mechanism Exacerbating Post-MI Remodeling by Sleep Breathing Disorders

2022-09-09 | GSE137125 | GEO

Effects of two weeks of intermittent hypoxia on liver and adipose tissue in lean mice,

Project description:Lean mice were submitted to either normoxia (controls) or CIH (CIH+) for 14 days. We analyzed liver and epidydimal adipose tissue signatures using transcriptomic analysis.

2017-09-23 | GSE104128 | GEO

Chronic intermittent hypoxia inhibits the revascularization of the ischemic retina and aggravates neurodegeneration and neovascularization

Project description:Neovascular retinopathies and edema are sign threatening complications of ischemic retinopathies, such as retinopathy of prematurity (ROP) and diabetic retinopathy (DR). Sleep apnea that leads to chronic intermittent hypoxia (CIH) is an independent risk factor for severe disease, but the underlying mechanisms are unknown. Here we show that experimental CIH during the ischemic phase of oxygen induced retinopathy in mice severely reduces beneficial revascularitzation of the ischemic retina, and increases neuronal loss and pathological neovascularization. Mechanistically we demonstrate that CIH reduces both colony stimulation factor 1 (CSF-1) expression and the ischemia-induced increase of retinal microglial cells that promotes the revascularization of the ischemic retina in the absence of CIH. Local CSF1R inhibition during ischemic retinopathy reduced the number of microglial cells, inhibited revascularization, and exacerbated pathological neovascularization, recapitulating several effects of CIH. Our findings provide a novel mechanism by which sleep apnea and CIH aggravate ischemic retinopathies, underscoring the importance of treating apnea in ROP and DR to help prevent sight threatening severe disease.

2025-03-19 | GSE268420 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data