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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE138008 | GEO | 2019/09/25

REPOSITORIES: GEO

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

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

2022-09-09 | GSE137125 | GEO

Expression data of Sham and post-MI myocardium from swine

Project description:The molecular mechanism underlying cardiac remodeling following myocardial infarction have been incompletely understood. Until now, most studies have been performed in rodents. We studied cardiac remodeling in the physiologically more relevant animal model, the swine. Microarray analysis was performed on animals that underwent either sham surgery or permanent ligation of the left coronary artery (MI). RNA was isolated from the remote, non-ischemic, regions of the left ventricle. RNA was isolated from 8 sham and 8 MI animals three weeks after surgery. Each group contained 4 males and 4 females. Animals used for the study were 2-3 months old Yorkshire x Landrace swine. Only neutered males entered the study.

2011-12-21 | E-GEOD-27962 | biostudies-arrayexpress

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

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

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Direct in vivo cardiac reprogramming improves cardiac function and ventricular remodeling in chronic MI.

Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in acute and chronic MI. Here we show that in vivo cardiac reprogramming improved cardiac function, and reversed cardiac remodeling in chronic MI using a novel transgenic mouse system. Transcriptome analysis revealed that in vivo cardiac reprogramming suppressed signs of fibrosis and inflammation. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.

2024-07-01 | GSE240310 | GEO

Gene expression of cardiac fibroblasts post-MI

Project description:Cardiac fibroblasts stay relatively quiescent under normal condition. These cells differentiate to myofibroblasts after myocardial infarction (MI), characterized by the expression of contractile proteins and secretion of elevated levels of extracellular matrix proteins, leading to cardiac remodeling. The differentiated myofiroblasts gradually lose most myofibroblast phenotypes but still persist in the infarct area to maintain the tissue structural integrity. We used microarrays to reveal the change in cardiac fibroblast gene expression profile after MI.

2018-02-24 | GSE111059 | GEO

RNA sequencing of rodent myocardial tissue when subjected to a myocardial infarction (MI) or an MI and a surgical device (TRD) for 12 weeks.

Project description:Purpose: The goal of this study is to compare mRNA related cellular pathways associated with a myocardial infarction (MI) with a surgical device to prevent cardiac remodeling compared to an MI only Conclusions: RNA sequencing revealed an activation of multiple cellular pathways with the device group.

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

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

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Expression data of Sham and post-MI myocardium from swine

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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

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