Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic sequencing of atrial fibrosis rat model caused by chronic intermittent hypoxia

ABSTRACT: This study was aimed to understand the changes of proteins occurring in atrial tissue of atrial fibrillation (AF) rat model based on proteome sequencing.SD rats were used for AF model construction by chronic intermittent hypoxia (CIH) induction. The tissue pathological changes were observed by hematoxylin-eosin staining, masson staining, and immunohistochemistry analysis of the levels of fibrosis biomarkers. Then proteome sequencing was performed on atrial fibrosis samples to identify the differentially expressed proteins (DEPs) between CIH and control groups, following by functional analysis. The protein levels of several key proteins were validated by western blotting.

ORGANISM(S): Rattus Norvegicus

SUBMITTER: Xue Liang

PROVIDER: PXD042312 | iProX | Thu May 18 00:00:00 BST 2023

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

Proteomic sequencing analysis in a rat model of atrial fibrosis caused by chronic intermittent hypoxia.

Zhao Bo B Wang Hualing H Cheng Lijun L Wang Manman M Li Jiao J Gu Tianshu T Shangguan Wenfeng W Miao Shuai S Wang Weiding W Liu Xing X Guan Siyu S Liu Tong T Liang Xue X

Journal of thoracic disease 20230922 10

<h4>Background</h4>Atrial fibrosis caused by long-term atrial fibrillation influences the outcomes of clinical treatment. An improved understanding of the mechanisms underlying atrial fibrillation may reveal new therapeutic targets. This study was conducted to analyze the changes in protein levels in the atrial tissue of a rat model of atrial fibrillation based on proteome sequencing.<h4>Methods</h4>Sprague-Dawley rats were used to develop a model of atrial fibrillation induced by chronic interm ...[more]

PMID: 37969261

Similar Datasets

Atrial Fibrillation After Surgery for Colorectal Cancer

Project description:This study will report the incidence of atrial fibrillation after elective colorectal cancer resection in the over 65 age group. This will be used to validate a risk model for the development of post-operative atrial fibrillation. Eligible patients will undergo electrocardiogram based screening for atrial fibrillation, as well as brain natriuretic peptide tests prior to surgery. They will undergo 24 hour holter monitor prior to surgery, and at 30 and 90 days following surgery. The primary outcome will be occurrence of atrial fibrillation within 90 days of surgery. Secondary outcomes include quality of life change, use of hospital services for atrial fibrillation, and complications of atrial fibrillation. This will be used to validate the pre-existing model for prediction of atrial fibrillation.

| 2312263 | ecrin-mdr-crc

Rac1-Induced Connective Tissue Growth Factor regulates Connexin 43 and N-Cadherin Expression in Atrial Fibrillation

Project description:Objectives: We studied the signal transduction of atrial structural remodelling that contributes to the pathogenesis of atrial fibrillation (AF). Backround: Fibrosis is a hallmark of arrhythmogenic structural remodelling but the underlying molecular mechanisms are incompletely understood. Methods: We performed transcriptional profiling of left atrial myocardium (LA) from patients with AF and sinus rhythm (SR) and applied cultured primary cardiac cells and transgenic mice with overexpression of constitutively active V12Rac1 (RacET) who develop AF at old age to characterize mediators of the signal transduction of atrial remodeling. Results: LA from patients with AF showed a marked upregulation of connective tissue growth factor (CTGF) expression compared SR patients. This was associated with increased fibrosis, NADPH-oxidase-, Rac1- and RhoA activity, upregulation of N-cadherin and connexin 43 (Cx43) expression and increased angiotensin II tissue concentration. In neonatal rat cardiac myocytes and -fibroblasts, a specific small molecule inhibitor of Rac1 or simvastatin completely prevented the angiotensin II induced upregulation of CTGF, Cx43 and N-cadherin expression. Transfection with small-inhibiting CTGF RNA blocked Cx43 and N-cadherin expression. RacET mice showed upregulation of CTGF, Cx43 and N-cadherin protein expression. Inhibition of Rac1 by oral statin treatment prevented these effects, identifying Rac1 as a key regulator of CTGF in vivo. Conclusion: The data identify CTGF as an important mediator of atrial structural remodelling during AF. Angiotensin II activates CTGF via activation of Rac1 and NADPH oxidase, leading to upregulation of Cx43, N-cadherin and interstitial fibrosis and therefore contributing to the signal transduction of atrial structural remodelling. Array design study consists of 5 Atrial Fibrillation patients and matched 5 samples of patients in sinus rhythm (controls).

2010-02-21 | E-GEOD-14975 | biostudies-arrayexpress

Effect of exercise at different loads in gene expression of both atria in male rats

Project description:Strenuous exercise increases the risk of atrial fibrillation, while moderate physical activity has been suggested to decrease its risk, Data from animal models suggest that intensive exercise, but not moderate training, increases atrial fibrosis and could be on the basis of the increased atrial fibrillation risk. The impact of the transition from moderate to strenuous exercise on atrial fibrillation risk and its underlying mechanisms remain poorly understood. We aimed to analyze biatrial remodeling after moderate and strenuous exercise. We conducted an RNA microarray of right and left atria of sedentary, mdoeratel-trained, and intensively-trained rats to uncover the mechanisms leading to atrial fibrosis in intensively trained rats.

2025-05-16 | GSE289211 | GEO

Therapeutic silencing Spp1 in cardiac macrophages suppresses atrial fibrillation

Project description:Atrial fibrillation (AFib) and the risk of its lethal complications are worsened by atrial fibrosis. A recent study implicates osteopontin (encoded by Spp1) secreted by atrial TREM2+ macrophages in this fibrosis. Here, we show that silencing Spp1 in TREM2+ cardiac macrophages using an antibody-siRNA conjugate (ARC) reduces atrial fibrosis and suppresses AFib, thus offering a new immunotherapy for this common arrhythmia.

2024-09-12 | GSE272503 | GEO

The role of stromal and immune cells in atrial disease [III]

Project description:In atrial fibrillation, disturbed electrical conduction disrupts the coordinated contraction of the heart’s antechambers, increasing the risk of stroke and heart failure. The rising prevalence of this disease approaches 9% in patients >65 years. Studying freshly isolated human atrial tissue and a new mouse model, we here decipher how immune and stromal cells contribute to the structural tissue remodeling that underlies atrial fibrillation. Single-cell transcriptomes from control and diseased human atria documented macrophage doubling at the expense of endothelial and mural cells. An inflammatory monocyte and a pro-fibrotic SPP1+ macrophage cluster expanded in patients with atrial fibrillation. To experimentally perturb pathways observed in patients, we matched their risk factors Hypertension, Obesity and Mitral valvE Regurgitation (HOMER) in mice. Atrial single-cell transcriptomes obtained in HOMER mice, which developed enlarged, fibrillation-prone atria, recapitulated human cell composition and transcriptome variations. Recruitment drove the expansion of atrial macrophages; accordingly, inhibition of monocyte migration reduced arrhythmia in Ccr2-/- HOMER mice. Deleting Spp1 established macrophage-derived osteopontin as a pleiotropic signal that promotes atrial fibrillation through pro-fibrotic, inflammatory crosstalk with an arsenal of local immune and stromal cells. Taken together, we identify SPP1+ macrophages as targets for immunomodulatory therapy in atrial fibrillation.

2023-07-13 | GSE225671 | GEO

The role of stromal and immune cells in atrial disease [I]

2023-07-13 | GSE197518 | GEO

The role of stromal and immune cells in atrial disease [II]

2023-07-13 | GSE224947 | GEO

Dysregulation of adipocytokines regulated by hsa-miR-548ay-3p/PPARγ signaling pathway leaded to cardiac fibrosis

Project description:Cardiac fibrosis is the key to the onset of atrial fibrillation (AF), but the mechanism is not fully understood. Our previous study found that fibrosis-related adipocytokines were dysregulated in epicardial adipose tissue (EAT) from patients with AF. In this study, we explored the factor that induce adipocytokines dysregulation and the mechanism underlying adipocytokines dysregulation-induced cardiac fibrosis.

2025-01-30 | GSE288419 | GEO

Human atrial tissue modification of Lysine 2-hydroxyisobutyrylation

Project description:The role of modification of histone lysine 2-hydroxyisobutyrylation in atrial fibrillation is unclear and we hence explored the role of 2-hydroxyisobutyrylation in atrial fibrillation. Tandem Mass Tag proteomics method and other verification technologies in tissues and cells identified the protein profiles and the regulation of 2-hydroxyisobutyrylation sites. The atrial tissue of the patients with atrial fibrillation has significant differences in modification of 2-hydroxyisobutyrylation compared to that in sinus rhythm.

2025-05-06 | PXD032154 | Pride

Transcriptional changes associated with advancing stages of heart failure underlie atrial and ventricular arrhythmogenesis underlie atrial and ventricular arrhythmogenesis

Project description:Heart failure (HF) is a leading cause of mortality and is associated with cardiac remodeling. Vulnerability to atrial fibrillation (AF) has been shown to be greater in the early stages of HF, whereas ventricular tachycardia/fibrillation develop during late stages. Here, we explore changes in gene expression that underlie the differential development of fibrosis and structural alterations that predispose to atrial and ventricular arrhythmias.

2019-01-01 | GSE123823 | 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