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RNA sequencing of rodent myocardial tissue when subjected to mitral regurgitation (MR) for different time-points, compared to normal Sham tissue.

ABSTRACT: RNA sequencing of rodent myocardial tissue when subjected to mitral regurgitation (MR) for different time-points, compared to normal Sham tissue.

PROVIDER: PRJNA625039 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11539624_1.fastq.gz	Fastqsanger.gz
	SRR11539624_2.fastq.gz	Fastqsanger.gz
	SRR11539625_1.fastq.gz	Fastqsanger.gz
	SRR11539625_2.fastq.gz	Fastqsanger.gz
	SRR11539626_1.fastq.gz	Fastqsanger.gz

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RNA sequencing of rodent myocardial tissue when subjected to mitral regurgitation (MR) for different time-points, compared to normal Sham tissue.

Project description:Purpose: The goal of this study is to compare mRNA related cellular pathways associated with mitral regurgitation compared to Sham Methods: RNA was extracted from myocardial tissue at 2, 10, 20, 40 weeks after MR surgery (n=5 samples/time-point) and was subjected to unbiased RNA sequencing. Conclusions: RNA sequencing revealed an early activation of multiple cellular pathways.

2020-11-30 | GSE148559 | GEO

Integration of functional imaging, cytometry and unbiased proteomics reveals new features of endothelial-to-mesenchymal transition in ischemic mitral valve regurgitation in human patients

Project description:Background: Following myocardial infarction, mitral regurgitation (MR) is a common complication. Previous animal studies demonstrated the association of endothelial-to-mesenchymal transition (EndMT) with mitral valve (MV) remodeling. Nevertheless, little is known about how MV tissue responds to ischemic heart changes in humans. Methods: MVs were obtained by the Cardiothoracic Surgical Trials Network from 17 patients with ischemic mitral regurgitation (IMR). Echo-doppler imaging assessed MV function at time of resection. Cryosections of MVs were analyzed using a multi-faceted histology and immunofluorescence examination of cell populations. MVs were further analyzed using unbiased label-free proteomics. Echo-Doppler imaging, histo-cytometry measures and proteomic analysis were then integrated. Results: MVs from patients with greater MR exhibited proteomic changes associated with proteolysis-, inflammatory- and oxidative stress-related processes compared to MVs with less MR. Cryosections of MVs from patients with IMR displayed activated valvular interstitial cells (aVICs) and double positive CD31+ αSMA+ cells, a hallmark of EndMT. Univariable and multivariable association with echocardiography measures revealed a positive correlation of MR severity with both cellular and geometric changes (e.g., aVICs, EndMT, leaflet thickness, leaflet tenting). Finally, proteomic changes associated with EndMT showed gene-ontology enrichment in vesicle-, inflammatory- and oxidative stress-related processes. This discovery approach indicated new candidate proteins associated with EndMT regulation in IMR. Conclusion: We describe an atypical cellular composition and distinctive proteome of human MVs from patients with IMR, which highlighted new candidate proteins implicated in EndMT-related processes, associated with maladaptive MV fibrotic remodeling.

2021-08-13 | PXD025096 | Pride

Mitral valve leaflet response to ischemic mitral regurgitation: From gene expression to tissue remodeling

Project description:Mitral valve leaflet response to ischemic mitral regurgitation: From gene expression to tissue remodeling

| PRJNA587626 | ENA

mTOR signal in mitral valve diseases

Project description:Mitral valve prolapse (MVP) is often benign but can progress to mitral regurgitation, requiring invasive treatment. In mgR mice with hypomorphic Fbn1 mutations—mimicking Marfan syndrome—myxomatous mitral degeneration and regurgitation develop by 12 weeks. TGF-β and mTOR signaling activation, along with macrophage infiltration, appear by 4 weeks, before histological changes. Short-term rapamycin treatment blocks early TGF-β activation and inflammation, while long-term mTOR or TGF-β inhibition rescues valve degeneration. Transcriptomics revealed integrins as upstream regulators of mTOR. Blocking integrin signaling or altering its pathway prevented mTOR activation. These findings are conserved in human MVP, suggesting that mTOR activation via abnormal integrin-matrix signaling drives disease and that mTOR inhibition may be a potential therapy.

2025-05-07 | GSE293926 | GEO

Expression data from Sus scrofa atria

Project description:Regulatory Mechanisms of Atrial Remodeling of Mitral Regurgitation Pigs This study enrolled 6 pigs (age: 18 months) and divided into three groups: mitral regurgitation pigs (MR) (n = 2; 2 males sacrificed 12 months after surgery), MR pigs treated with valsartan (MRV) (n = 2; 2 males age-matched to MR sacrificed 12 months after surgery), and normal control pigs (NC) (n = 2; 2 males age-matched to MR pigs). Valsartan (3.43 mg/kg/day), a type I angiotensin II receptor blocker, was administered from one week before surgery and then daily after surgery in the MRV group. We sought to systemically elucidate critical differences in the alteration of RNA expression pattern between the atrial myocardium of pigs with and without MR, and between the atrial myocardium of MR pigs with and without valsartan using high-density oligonucleotide microarrays and functional network enrichment analysis.

2015-02-01 | E-GEOD-43072 | biostudies-arrayexpress

Exploring Regulatory Mechanisms of Atrial Myocyte Hypertrophy of Mitral Regurgitation through Gene Expression Profiling Analysis: Role of NFAT in Cardiac Hypertrophy

Project description:Regulatory Mechanisms of Atrial Remodeling of Human Mitral Regurgitation

2016-11-07 | GSE63045 | GEO

Single-cell analysis reveals the loss of progenitor subpopulation of valvular endothelial cells leads to functional mitral regurgitation

Project description:We conducted single-cell RNA sequencing analysis of mitral valve leaflets extracted from six patients, comprising three individuals with moderate-to-severe functional mitral regurgitation and three nondiseased mitral valve controls. Bioinformatics was used to identify the cell types, describe the cell functions, and investigate cellular developmental trajectories and interactions.

2024-12-27 | GSE241947 | GEO

Myocardial proteome profiling reveals disease- and sex-specific alterations in patients with aortic valve stenosis and mitral valve regurgitation

Project description:Heart valve diseases, such as aortic valve stenosis (AS) and mitral valve regurgitation (MR), are leading causes of heart failure. However, myocardial proteome studies in AS and MR are extremely rare. We profiled the proteome of 75 human left ventricular myocardial biopsies (AS=41, MR=17, controls=17) and detected disease- and sex-specific protein expression alterations. Patients with AS, for example, showed higher abundance of fibrosis-related proteins and lower abundance of proteins related to energy metabolism and protein synthesis capacity with prominent sex differences. This might explain the higher amount of myocardial mass and fibrosis and lower systolic cardiac function especially observed in male AS in our cohort and might help to find specific proteins as treatment targets. Our work provides detailed insight into myocardial protein alterations in AS and MR and expands, in combination with clinical parameters, the understanding of cardiac remodeling in female and male patients, aiming to improve disease- and sex-specific therapy.

2022-12-13 | PXD023800 | Pride

Normal human mitral valve proteome: a preliminary investigation by gel-based and gel-free proteomic approaches

Project description:The mitral valve is a highly complex structure which regulates blood flow from the left atrium to the left ventricle (LV) avoiding a significant forward gradient during diastole or regurgitation during systole. The integrity of the mitral valve is also essential for the maintenance of normal LV size, geometry, and function. Significant advances in the comprehension of the biological, functional, and mechanical behavior of the mitral valve have recently been made. However, current knowledge of protein components in the normal human mitral valve is still limited and complicated by the low cellularity of this tissue and the presence of high abundant proteins from the extracellular matrix. We employed here an integrated proteomic approach to analyse the protein composition of the normal human mitral valve and reported confident identification of 422 proteins, some of which have not been previously described in this tissue. In particular, we described the ability of pre-MS separation technique based on liquid-phase IEF and SDS-PAGE to identify the largest number of proteins. These initial results provide a valuable basis for future studies aimed at analysing in depth the mitral valve protein composition and at investigating potential pathogenetic molecular mechanisms.

2016-08-18 | PXD004397 | Pride

Differential Requirement for DICER1 Activity during the Development of Mitral and Tricuspid Vlaves

Project description:Mitral and tricuspid valves are essential for unidirectional blood flow in the heart. They are derived from similar cell sources, and yet congenital dysplasia affecting both valves is clinically rare, suggesting the presence of differential regulatory mechanisms underlying their development. We specifically inactivated Dicer1 in the endocardium during cardiogenesis and found that Dicer1-deletion caused congenital mitral valve stenosis and regurgitation, while it had no impact on other valves. We showed that hyperplastic mitral valves were caused by abnormal condensation and extracellular matrix (ECM) remodeling. Our single-cell RNA Sequencing analysis revealed impaired maturation of mesenchymal cells and abnormal expression of ECM genes in mutant mitral valves. Furthermore, expression of a set of miRNAs that target ECM genes was significantly lower in tricuspid valves compared to mitral valves, consistent with the idea that the miRNAs are differentially required for mitral and tricuspid valve development. We thus reveal miRNA-mediated gene regulation as a novel molecular mechanism that differentially regulates mitral and tricuspid valve development, thereby enhancing our understanding of the non-association of inborn mitral and tricuspid dysplasia observed clinically.

2022-08-19 | GSE207226 | GEO

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