NHLBI TOPMed: HyperGEN - Genetics of Left Ventricular (LV) Hypertrophy
Ontology highlight
ABSTRACT: The Hypertension Genetic Epidemiology Network Study (HyperGEN) - Genetics of Left Ventricular (LV) Hypertrophy is a familial study aimed to understand genetic risk factors for LV hypertrophy by conducting genetic studies of continuous traits from echocardiography exams. The originating HyperGEN study aimed to understand genetic risk factors for hypertension. Data from detailed clinical exams as well as genotyping data for linkage studies, candidate gene studies and GWAS have been collected and is shared between HyperGEN and the ancillary HyperGEN - Genetics of LV Hypertrophy study.
SECONDARY ACCESSION(S): PRJNA371675PRJNA371676
REPOSITORIES: dbGaP
Similar Datasets
Project description:Diet induced obesity in rat was associated with myocardial dysfunction, hypertension and fibrosis. This study aimed to explore microRNA expression profiles in diet obesity-induced rat myocardium. Wistar rats were feed normal chow or high-fat diet for 20 weeks. After that, cardiac function was evaluated by echocardiography. Left ventricular myocardium was harvest to assess the extent of hypertension and fibrosis, meanwile, the left ventricular microRNA expression was analyzed using Agilent Rat miRNA microarray. Significant cardiac dysfunction, hypertension and fibrosis were found in diet-induced obesity rats as compared with normal diet rats. rno-miR-141-3p and rno-miR-144-3p were also significantly increased in myocardium of diet-induced obesity rat. These findings suggest that specific miRNA differences may contribute to the alteration in cardiac function, hypertension and fibrosis which responses to diet-induced obesity.
2020-01-07 | GSE143168 | GEO
Project description:Arterial pulmonary hypertension is a rare disease, with little knowledge regarding its etiology, and high mortality. Development of right and later on also left ventricular heart insufficiency, secondary to pulmonary hypertension, is a negative predictive factor. Genetic and molecular processes underlying left heart ventricle remodeling over the course of pulmonary hypertension remain unknown. In particular, there is no knowledge regarding the mechanisms of left heart ventricle atrophy which was completely avoided by researchers until recently.The aim of this study was to assess changes in protein abundance in left and right heart ventricle free wall of rats in monocrotaline model of PAH.
2020-09-07 | PXD015896 | Pride
Project description:Analysis of the effects of aging on the development of dilated cardiomyopathy by characterizing both changes in ejection fraction (EF) and gene expression profile in 3 groups of male mice: Control (Cont or WT, n=11) and transgenic (Tg or KO) mice with either high EF (KO-H or Tg-H, n=7) or low EF (KO-L or Tg-L, n=6). We previously produced a line of transgenic mice (Tg) on a mixed genetic background where cardiac-specific overexpression of Cre recombinase reduced expression of the EP4 receptor gene. There were no obvious phenotypes in 10-12-week-old male Tg mice. To determine if a cardiac phenotype developed in aged mice, we assessed cardiac structure and function by echocardiography, histology and gene expression in 23-33-week-old male Tg and littermates (Cont). After echocardiography, hearts were removed to assess hypertrophy (MCSA), fibrosis (ICF) and macrophage infiltration by histological methods and for extraction of total RNA and protein. Cont mice had a normal EF of 80±0.6% (n=70), whereas Tg mice had a lower EF (60±2.7%, n=55, p<0.001) coupled with left ventricular dilatation. The distribution of EFs in the Tg mice was large, ranging from normal to below 30%. MCSA and infiltrating macrophages were not different between groups, but ICF increased by 35% in Tg mice. Cre protein levels in heart lysates did not correlate with either age or EF. In contrast to male Tg mice, female Tg mice had no cardiac dysfunction assessed by echocardiography from 12 to 28 weeks of age. To understand gene expression differences between Cont and Tg mice, whole genome gene expression profiling (Illumina BeadChips) on hearts of 30-32 week old male mice was done. Data indicated that 595 genes were overexpressed in the Tg hearts, 156 of which changed more than 2-fold, including genes involved in remodeling, inflammation, and oxidative stress. 512 genes were downregulated in the Cont hearts, 79 of which changed more than 2-fold, including genes involved with calcium handling, K+ channels, and fatty acid transport and metabolism. In conclusion, Cre overexpression and EP4 knock down in cardiac myocytes in aged male but not female Tg mice are in part associated with increased fibrosis, reduced EF and dilated cardiomyopathy; however, Cre protein itself does not seem to be responsible for the cardiomyopathy. The absence of cardiac dysfunction in female mice suggests a sexual dimorphism in the phenotype. Creation of the cardiac-myocyte specific EP4 KO mouse and littermate controls was described in JY Qian et al, Hypertension 2008: 51(pt 2):560-566. Total RNA extracted from left ventricle of control (Cont or WT, n =11) and cardiac-specific EP4 KO (Tg or KO, n=13) male mice (mean age 31 weeks).
2010-04-13 | E-GEOD-16909 | biostudies-arrayexpress
Project description:Although there have been studies conducted on cornea and retina growth and development, postnatal gene expression studies on sclera growth during postnatal growth has not been well characterised. Given that the mouse genome has 85% homology to the human genome and has been completely sequenced, mouse model for the study of ocular growth has advantages over other animal models. Thus, we aimed to study the biology and genetics behind sclera growth during post-natal development in Balb/cJ mice as a means to understand genetic changes that cause scleral growth and development during post-natal eye development The purpose of this study was to identify the genes underlying the development of mouse sclera post-natal growth of the posterior chamber of the eye using microarray
2011-03-22 | GSE28056 | GEO
Project description:Pulmonary hypertension worsens outcome in left heart disease. Stiffening of the pulmonary artery may drive this pathology by increasing right ventricular dysfunction and lung vascular remodeling. We showed that pulmonary arteries from patients with left heart disease are characterized by increased stiffness that correlates with impaired pulmonary hemodynamics. Pulmonary arteries in left heart disease patients with pulmonary hypertension were characterized by degradation of elastic fibers paralleled by an accumulation of fibrillar collagens. We utilized RNA sequencing to identify differentially expressed genes regulating extracellular matrix remodeling in pulmonary arteries of left heart disease patients with or without pulmonary hypertension, in comparison to healthy-heart donor controls. As such we identified that transcriptional deregulation of extracellular matrix constituents and their regulators precedes clinical pulmonary hypertension, and therefore might be a pathomechanism that drives pulmonary arterial remodeling and stiffening in left heart disease.
2023-07-03 | GSE236251 | GEO
Project description:We wanted to understand how a salt restriction diet could improve cardiac damage (ie cardiac hypertrophy, fibrosis, hypertension) in a rat model of metabolic syndrome. We thus performed an Agilent microarray experiment in order to identify expression variations in left ventricles of rats having a normal sodium diet (0,64%) or a low sodium diet (less than 0,01%)
2017-04-20 | GSE84524 | GEO
Project description:Pulmonary arterial hypertension (PAH) is a common and serious complication of left-to-right shunt congenital heart disease (CHD).Some studies have provided evidence indicating that various circRNAs are abnormally expressed in pulmonary hypertension. However, the diagnostic value and biological functions of circRNAs in PAH remain largely elusive. To study the potential roles of circRNAs in PAH, we performed microarray analysis to identify circRNAs differentially expressed between pediatric patients with PAH due to CHD and control subjects.
2021-04-11 | GSE171827 | GEO
Project description:Although there have been studies conducted on cornea and retina growth and development, postnatal gene expression studies on sclera growth during postnatal growth has not been well characterised. Given that the mouse genome has 85% homology to the human genome and has been completely sequenced, mouse model for the study of ocular growth has advantages over other animal models. Thus, we aimed to study the biology and genetics behind sclera growth during post-natal development in Balb/cJ mice as a means to understand genetic changes that cause scleral growth and development during post-natal eye development The purpose of this study was to identify the genes underlying the development of mouse sclera post-natal growth of the posterior chamber of the eye using microarray Total RNA was isolated from single cryogenically ground mouse sclera (n=30, 6 samples each from week 1-, 2-, 3-, 6-and 8-old mice), reverse-transcribed and hybridized onto a Affymetrix mouse gene 1.0 ST array.We sought to use microarray to determine the gene expression profiles of mouse sclera from different age groups and identify the developmental genes that are involved in postnatal ocular growth.
2011-03-22 | E-GEOD-28056 | biostudies-arrayexpress
Project description:Proteins perform a wide range of biological functions and are often exhibit to multi-factorial regulatory patterns. To better understand the roles of genetics and sex in protein regulation, we quantitatively analyze and compare the liver proteomes from related genetically diverse mouse populations, representing inbred genetic backgrounds.
2021-07-29 | PXD018886 | Pride
Project description:Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF. We used microarrays to investigate gene expression in the left ventricle (LV) accompanying myocardial infarction and concomitant heart failure (HF) in a well validated model of post-infarcted heart failure and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs) Myocardial infarction (MI) was induced in male Wistar rats by ligation of the proximal left coronary artery. The sham-operated group (control group) was subjected to the same protocol, except that the suture was not tied around the proximal left coronary artery. Sham-operated rats (n=6) and rats with small (n=6), moderate (n=6), and large (n=5) MI size were included into the experiment two months after the operation. Then, left ventricules and blood samples were obtained for RNA extraction and hybridization on Affymetrix microarrays. Microarrays were used to compare the LV and PBMCs transcriptomes of control and experimental animals. The development of heart failure was estimated by echocardiography and catheterization.
2013-11-15 | E-GEOD-47495 | biostudies-arrayexpress