E-GEOD-37922
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-37922 | ExpressionAtlas | 2015-07-27
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-37922-analysis-methods.tsv | Tabular | |||
| E-GEOD-37922-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-37922-configuration.xml | Xml | |||
| E-GEOD-37922-percentile-ranks.tsv | Tabular | |||
| E-GEOD-37922.condensed-sdrf.tsv | Tabular |
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Project description:: The adult heart develops hypertrophy to reduce ventricular wall stress and maintain cardiac function in response to an increased workload. Although pathological hypertrophy generally progresses to heart failure, physiological hypertrophy may be cardioprotective. Cardiac-specific overexpression of the lipid-droplet protein perilipin 5 (Plin5) promotes cardiac hypertrophy, but it is unclear if this response is beneficial. We analyzed human RNA-sequencing data from the left ventricle and showed that cardiac PLIN5 expression correlates with upregulation of cardiac contraction-related processes. To investigate how elevated cardiac Plin5 levels affect cardiac contractility, we generated mice with cardiac-specific overexpression of Plin5 (MHC-Plin5 mice). These mice displayed increased left ventricular mass and cardiomyocyte size but preserved heart function. Quantitative proteomics identified sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) as a Plin5-interacting protein. Phosphorylation of phospholamban, the master regulator of SERCA2, was increased in MHC-Plin5 versus wild-type cardiomyocytes. Live imaging showed increases in intracellular Ca2+ release during contraction, Ca2+ removal during relaxation, and SERCA2 function in MHC-Plin5 versus wild-type cardiomyocytes. These results identify a role for Plin5 in improving cardiac contractility through enhanced Ca2+ signaling.
2023-01-20 | PXD035121 | Pride
Project description:Cardiovascular disease (CVD) in chronic kidney disease (CKD) is characterized by vascular calcification and cardiac remodeling. CKD induced cardiac hypertrophy precedes cardiac fibrosis and is associated with left ventricular dysfunction. Elevated phosphate concentration due to renal failure is known to be involved in cardiac remodeling.
2016-10-25 | GSE89130 | GEO
Project description:We report, for the first time, engineering of heteropolar cardiac tissues containing distinct atrial and ventricular ends, and demonstrate their spatially confined responses to serotonin and ranolazine. Uniquely, electrical conditioning for up to 8 months enabled modeling of polygenic left ventricular hypertrophy starting from patient cells.
2018-12-13 | GSE122661 | GEO
Project description:BACKGROUND: Cardiac hypertrophy compensates for increased biomechanical stress of the heart induced by prevalent cardiovascular pathologies, but can result in cardiac failure if left untreated. We hypothesized that the tail-anchored protein Dysferlin with multiple Ca2+-binding C2-domains is critical for the integrity of the transverse-axial tubule (TAT) network inside cardiomyocytes, and contributes to the proliferation of TAT endomembranes during pressure overload-induced cardiac hypertrophy. OBJECTIVE: To reveal the impact of the membrane fusion and repair protein Dysferlin on TAT network stabilization and proliferation necessary for the hypertrophic growth of cardiomyocytes. METHODS AND RESULTS: Super-resolution light and electron microscopy of mouse cardiomyocytes identified a specific localization of Dysferlin in a vesicular compartment in nanometric proximity to contact sites of the TAT network with the sarcoplasmic reticulum (SR), a.k.a. junctional complexes for Ca2+-induced Ca2+ release. Mass spectrometry was used to characterize the cardiac Dysferlin interactome, thereby identifying a novel protein interaction with the membrane-tethering SR protein Juncophilin-2, a known interactor of L-type Ca2+ channels and Ryanodine Receptor Ca2+ release channels in junctional complexes. While the Dysferlin knockout caused a mild progressive phenotype of dilated cardiomyopathy in the mouse heart, global proteome analysis revealed changes preceding systolic failure. Following transverse aortic constriction (TAC), Dysferlin protein expression was significantly increased in hypertrophied wild-type myocardium, while Dysferlin knockout animals presented markedly reduced left-ventricular hypertrophy. Live-cell membrane imaging demonstrated a profound reorganization of the TAT network in wild-type left-ventricular myocytes post-TAC with robust proliferation of axial tubules, which critically depended on the increased expression of Dysferlin within newly-emerging tubule components. CONCLUSIONS: Dysferlin represents a new molecular target in cardiac disease that protects the integrity of tubule-SR junctional complexes for regulated excitation-contraction coupling, and controls TAT network reorganization and tubular membrane proliferation in cardiomyocyte hypertrophy induced by pressure-overload.
2024-07-15 | PXD053051 | Pride
Project description:BACKGROUND: Cardiac hypertrophy compensates for increased biomechanical stress of the heart induced by prevalent cardiovascular pathologies, but can result in cardiac failure if left untreated. We hypothesized that the tail-anchored protein Dysferlin with multiple Ca2+-binding C2-domains is critical for the integrity of the transverse-axial tubule (TAT) network inside cardiomyocytes, and contributes to the proliferation of TAT endomembranes during pressure overload-induced cardiac hypertrophy. OBJECTIVE: To reveal the impact of the membrane fusion and repair protein Dysferlin on TAT network stabilization and proliferation necessary for the hypertrophic growth of cardiomyocytes. METHODS AND RESULTS: Super-resolution light and electron microscopy of mouse cardiomyocytes identified a specific localization of Dysferlin in a vesicular compartment in nanometric proximity to contact sites of the TAT network with the sarcoplasmic reticulum (SR), a.k.a. junctional complexes for Ca2+-induced Ca2+ release. Mass spectrometry was used to characterize the cardiac Dysferlin interactome, thereby identifying a novel protein interaction with the membrane-tethering SR protein Juncophilin-2, a known interactor of L-type Ca2+ channels and Ryanodine Receptor Ca2+ release channels in junctional complexes. While the Dysferlin knockout caused a mild progressive phenotype of dilated cardiomyopathy in the mouse heart, global proteome analysis revealed changes preceding systolic failure. Following transverse aortic constriction (TAC), Dysferlin protein expression was significantly increased in hypertrophied wild-type myocardium, while Dysferlin knockout animals presented markedly reduced left-ventricular hypertrophy. Live-cell membrane imaging demonstrated a profound reorganization of the TAT network in wild-type left-ventricular myocytes post-TAC with robust proliferation of axial tubules, which critically depended on the increased expression of Dysferlin within newly-emerging tubule components. CONCLUSIONS: Dysferlin represents a new molecular target in cardiac disease that protects the integrity of tubule-SR junctional complexes for regulated excitation-contraction coupling, and controls TAT network reorganization and tubular membrane proliferation in cardiomyocyte hypertrophy induced by pressure-overload.
2024-07-15 | PXD053037 | Pride
Project description:Aortic banding is an excellent model system to evaluate the process of development of left ventricular hypertrophy in response to hemodynamic stress. The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different time points after surgical intervention for pressure-overload induced hypertrophy. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/band_home.html Keywords = Pressure overload, cardiac hypertrophy Keywords: time-course
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Project description:To evaluate the genome-wide changes in gene translational efficiency during the development of heart failure, we performed transverse aortic constriction(TAC) in male C57BL/6 mice. According to our experience, hypertrophy of the left ventricle was observed 2 weeks after TAC. Cardiac decompensation was observed at 5 weeks. We collected left ventricular tissues at 0, 2, 5 weeks after TAC and then performed ribosome footprinting and sequencing.
2023-10-31 | E-MTAB-8552 | biostudies-arrayexpress
Project description:BACKGROUND - MicroRNAs (miRs) are a class of small non-coding RNAs that regulate gene expression. Transgenic models have proved that a single miR can induce pathological cardiac hypertrophy and failure. The roles of miRs in the genesis of physiologic left ventricular hypertrophy (LVH), however, are not well elucidated. OBJECTIVE - To evaluate miRs expression in an experimental model of exercise-induced LVH. METHODS - Male Balb/c mice were divided into sedentary (SED) and exercise (EXE) groups. Voluntary exercise was performed in odometer-monitored metal wheels during 35 days. Analyses were performed after 7 and 35 days of training, and consisted of transthoracic echocardiography, maximal exercise test, miRs microarray (miRBase v.16) and real-time qRT-PCR analysis. RESULTS - Left ventricular weight/body weight ratio increased by 7% in the EXE group at day 7 (p<0.01) and by 11% at 35 days of training (p<0.001) After 7 days of training, microarray identified 35 deregulated miRs: 20 had an increase in their expression and 15 were down-regulated (p=0.01). At day 35 of training, 25 miRs were deregulated: 15 were up-regulated and 10 had decreased their expression compared to the SED group (p<0.01). qRT-PCR confirmed an increase in miR-150 levels at both time points and a decrease in miR-26b, miR-27a and miR-143 after 7 days of voluntary exercise. CONCLUSIONS M-bM-^@M-^S We unraveled new miRs that can modulate physiological cardiac hypertrophy, particularly miR-26b, -150, 27a and -143. Our data also indicate that previously established regulatory gene pathways involved in pathological LVH are not deregulated in physiologic LVH. Experimental model of left ventricular hypertrophy induced by voluntary exercise Male Balb/c mice, 8-10 weeks old, 4 groups analyzed, each group consisted of a pool from 4 animals
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