Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA117777 | ENA |
REPOSITORIES: ENA
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Project description:Aortic valve regurgitation (AR) imposes a severe volume overload to the left ventricle (LV) which results in dilation, eccentric hypertrophy and eventually loss of function. Little is known about the impact of AR on LV gene expression. We therefore conducted a gene expression profiling study in the LV of male Wistar rats with chronic (9 months) and severe AR. Five male Wistar rats had one or two aortic valve leaflets punctured with a catheter under echocardiographic guidance in order to induce severe regurgitation (>65% of blood regurgitating during diastole from the aorta to the left ventricle). Five additional rats were sham-operated. The animals were sacrificed 9 months after the procedure and their left ventricle collected for RNA extraction and microarray analysis.
2010-04-13 | E-GEOD-17050 | biostudies-arrayexpress
Project description:Aortic valve regurgitation (AR) imposes a severe volume overload to the left ventricle (LV) which results in dilation, eccentric hypertrophy and eventually loss of function. Little is known about the impact of AR on LV gene expression. We therefore conducted a gene expression profiling study in the LV of male Wistar rats with chronic (9 months) and severe AR.
2010-03-31 | GSE17050 | GEO
Project description:We aimed to disclose specific LV myocardial protein signatures possibly contributing to differential disease progression after aortic valve surgery in patients with chronic aortic stenosis and patients with chronic aortic regurgitation.
2023-05-10 | PXD039662 | Pride
Project description:Objectives: Diseased animal models play a crucial role in understanding of the mechanisms and identifying therapeutic targets of human diseases. Left ventricular pressure overload (LVPO) is common in children with various types of cardiovascular diseases, such as aortic valve stenosis and hypertension. However, the current neonatal rat model of LVPO is limited in transverse aortic constriction (TAC) model, characterized by the fixed LVPO and rapid pathological progress of left ventricle, which are not in consistency with the progressive LVPO and relative slow pathological progress of left ventricle in the above pediatric cardiovascular diseases. The purpose of this study is to establish a neonatal rat model of progressive LVPO.
2025-08-20 | GSE289819 | GEO
Project description:Compared Gene Expression Profiling of Rats with Aortic valve Regurgitation (AR) vs Sham operated Rats
2009-06-10 | E-TABM-490 | biostudies-arrayexpress
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
Project description:To characterize a expression patterns in the heart, we used rat. 12 Wistar male rats (8 - 11 weeks) were sacrificed. Left atrium (LA) adjacent to the pulmonary vein (PV), a mass of left ventricle (LV), and free-wall of the right ventricle (RV) was isolated. Each LV mass was dissected into three pieces as samples. Because the SAN isolation procedure takes approximately 20 minutes, SA was isolated separately. The SA region was delimited by the borders of the crista terminalis, the interatrial septum, the superior vena cava, and right atrium (RA). In addition to PV, LV, RV, SA, and RA samples, pulmonary arteries were added to the samples for the rat microarray.
2022-06-22 | GSE203369 | GEO
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
Project description:Aortic valve stenosis (AS) is a serious condition characterized by the progressive narrowing of the aortic valve, associated with a continuous rise in left ventricle pressure overload. Currently, aortic valve replacement (AVR) remains as the definitive treatment for AS, since an immediate dissipation of left ventricle pressure overload is achieved with this intervention. Upon AVR, a myocardial response, known as reverse remodeling (RR), is set into motion, characterized by regression of hypertrophy and cardiac function normalization. In spite of the AVR benefits, cardiologists still face the problem of RR variability, with some patients displaying a complete and others an incomplete recovery, for instance, due to prevailing hypertrophy. Patients with incomplete RR are at higher risk of developing diastolic dysfunction and, ultimately, heart failure. Myocardial biopsies, available during AVR, provide a wealth of information through its molecular characterization. Particularly, the characterization of the myocardium phosphoproteome may help identify dysregulated pathways underlying an incomplete RR. Moreover, kinase prediction can also be useful to identify new molecular targets aiming at improving the phenotype of this subset of patients. Hence, we aimed to characterize, for the first time, the myocardial phosphoproteome from AS patients with complete and incomplete RR. To fulfil this task, we followed a shotgun LC-MS/MS approach using an Orbitrap instrument, after TiO2-based phosphopeptide enrichment. Phosphopeptides were identified and quantified through a MaxQuant label-free quantification approach (FDR 1%).
2025-10-20 | PXD015498 | Pride
Project description:Located at the junction of left ventricle and ascending aorta, aortic root is a central cardiovascular structure consisting of aortic valve and coronary ostium that are essential for systemic and coronary circulation, respectively. Malformations of aortic valve and coronary ostium are common birth defects and may occur together in human patients, leading to complex complications including aortic valve stenosis, myocardial ischemia, heart failure and sudden cardiac death. Despite of their physiological and clinical significances, the developmental and molecular mechanisms by which coordinate the formation of aortic valve and coronary ostium remain poorly understood. Here we report that SOX17 (SRY-box 17) is an essential transcription factor required for the maturation of aortic root, as well as the patterning of aortic valve and coronary ostium. We show in mouse that deletion of Sox17 in the aortic root endothelium results in defective aortic valve with underdeveloped non-coronary leaflet (NCL) or bicuspid aortic valve (BAV) without NCL. The valve defects are accompanied by misplaced left coronary ostium that reduces coronary blood flow, leading to myocardial hypoxia and death of embryos. Mechanistically, deletion of Sox17 decreases the expression of Pdgfb (Platelet derived growth factor, B polypeptide) in the aortic root endothelium and the PDGF growth signaling in the NCL mesenchyme and aortic root smooth muscle, both of which are derived from the second heart field (SHF) cardiomyocyte precursors. Furthermore, the deletion upregulates the expression of Ctgf (Connective tissue growth factor) and the extracellular matrix (ECM) genes, whereas downregulates the vascular smooth muscle genes, in the forming aortic root. Together, these findings support a developmental disease mechanism in which delayed growth and maturation of aortic root, due to lack of SOX17-PDGF/CTGF signaling, contributes to BAV and CAAs, two common congenital cardiovascular defects.
2022-04-09 | GSE129564 | GEO