Expression data from healthy and diastolic heart failure rats
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ABSTRACT:
PROVIDER: PRJNA520901 | ENA |
REPOSITORIES: ENA
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Project description:Heart failure (HF) with preserved ejection fraction (HFpEF) is rising, whose morbidity, mortality and healthcare costs are similar to HF with reduced ejection fraction (HFrEF). Although substantial molecular pathways lead to the changes in organ and tissue levels, there are still lack of successful treatments for HFpEF given the complexity molecular networks remaining unknown. Here we report that the significantly changed genes of HFpEF rats associates positively with inflammatory processes and immune responses while negatively with calcium ion transport into cytosol. GSEA analysis shows several KEGG pathways are significantly enriched in HFpEF rats including p53 signaling pathway, Toll like receptor signaling pathway and so on. Our study provides new insights into HFpEF pathogenesis and a new therapeutic against HFpEF.
2019-02-05 | GSE126062 | GEO
Project description:We aimed to identify gene variants associated with heart failure by using a rat model of the human disease. We performed invasive cardiac hemodynamic measurements in F2 crosses between spontaneously hypertensive heart failure rats (SHHF) and reference strains. We combined linkage analyses with genome-wide expression profiling .
2008-09-01 | E-TABM-418 | biostudies-arrayexpress
Project description:Rats overexpressing the human renin and angiotensinogen genes die after seven weeks of end organ damage. They develop hypertension, heart hypertrophy and proteinuria.We compared terminal heart failure, these are indeed terminally ill to double transgenic animals suffering on hypertension, proteinuria and heart hypertrophy. In addition, Losartan-treated animals (10 mg/kg/d)showed similar physiological parameters (normotension, no proteinuria and no heart hypertrophy compared to control sprague dawley rats.
2008-06-11 | E-GEOD-1557 | biostudies-arrayexpress
Project description:In the present study we aimed to investigate whether alterations in left ventricular myocardial micro-RNA (miRNA) expression and post-transcriptional gene regulation might contribute to the development of systolic heart failure in aortic-banded (AB) rats. Hence, in young adult male Sprague-Dawley rats abdominal AB was carried out. In 10% of the AB animals, congestive systolic heart failure developed after 12 weeks of follow-up. These rats made up the AB-heart failure group. On the other hand, in the majority of the AB rats (almost 90%), heart failure signs were not present. These rats made up the AB-hypertrophy group. Additionally, sham-operated animals served as controls. miRNA profiling was conducted in all the three experimental groups. Based on the NGS data, network theoretical miRNA-target analysis was than performed to predict target genes. The mRNA expression of the predicted genes were finally measured by qPCR.
2023-05-24 | E-MTAB-12671 | biostudies-arrayexpress
Project description:Rats overexpressing the human renin and angiotensinogen genes die after seven weeks of end organ damage. They develop hypertension, heart hypertrophy and proteinuria.We compared terminal heart failure, these are indeed terminally ill to double transgenic animals suffering on hypertension, proteinuria and heart hypertrophy. In addition, Losartan-treated animals (10 mg/kg/d)showed similar physiological parameters (normotension, no proteinuria and no heart hypertrophy compared to control sprague dawley rats. Keywords: other
2005-01-03 | GSE1557 | GEO
Project description:Background: Vitamin D deficiency is associated with cardiac hypertrophy and heart failure, and vitamin D therapy prevents the progression of cardiac hypertrophy in animal models. Here, we examine whether vitamin D therapy regresses pre-existing cardiac hypertrophy, and prevents the progression to heart failure. Methods and Results: When male Dahl salt-sensitive (DSS) rats are fed a high salt (HS) diet, all rats develop cardiac hypertrophy after 5 weeks (H). Thereafter, rats were treated with vehicle (V), paricalcitol (PC, an active vitamin D analog at 200ng, IP 3x/wk), enalapril (EP, 90ug/day), and PC+EP. All groups were continued on the HS diet and evaluated after 4 weeks of therapy. The PC and PC+EP, but not the V and EP-only groups, showed significant regression of pre-existing cardiac hypertrophy. The signs of decompensated heart failure were evident in the vehicle-treated group; these heart failure parameters significantly improved with PC, EP or PC+EP therapy. The expression of PKCe, which is regulated by Ca2+ and known to stimulate cardiac hypertrophy, was significantly increased in the vehicle group, and PC, EP or PC+EP effectively decreased PKCe activation. We also observed normalization of genetic alterations during progression to heart failure with PC treatment. Conclusions: PC treatment resulted in both the regression of pre-existing cardiac hypertrophy, and the attenuation of the progression to heart failure, compared to improvement in progression to heart failure by EP alone. These beneficial findings in the heart were associated with inhibition of PKCe activation, and reversal of gene alterations.
2010-09-14 | GSE24110 | GEO
Project description:Background: Vitamin D deficiency is associated with cardiac hypertrophy and heart failure, and vitamin D therapy prevents the progression of cardiac hypertrophy in animal models. Here, we examine whether vitamin D therapy regresses pre-existing cardiac hypertrophy, and prevents the progression to heart failure. Methods and Results: When male Dahl salt-sensitive (DSS) rats are fed a high salt (HS) diet, all rats develop cardiac hypertrophy after 5 weeks (H). Thereafter, rats were treated with vehicle (V), paricalcitol (PC, an active vitamin D analog at 200ng, IP 3x/wk), enalapril (EP, 90ug/day), and PC+EP. All groups were continued on the HS diet and evaluated after 4 weeks of therapy. The PC and PC+EP, but not the V and EP-only groups, showed significant regression of pre-existing cardiac hypertrophy. The signs of decompensated heart failure were evident in the vehicle-treated group; these heart failure parameters significantly improved with PC, EP or PC+EP therapy. The expression of PKCe, which is regulated by Ca2+ and known to stimulate cardiac hypertrophy, was significantly increased in the vehicle group, and PC, EP or PC+EP effectively decreased PKCe activation. We also observed normalization of genetic alterations during progression to heart failure with PC treatment. Conclusions: PC treatment resulted in both the regression of pre-existing cardiac hypertrophy, and the attenuation of the progression to heart failure, compared to improvement in progression to heart failure by EP alone. These beneficial findings in the heart were associated with inhibition of PKCe activation, and reversal of gene alterations. Male Dahl salt-sensitive rats (Harlan Sprague–Dawley, Somerville, NJ) were bred and fed a normal diet until 6 weeks of age. To generate pressure overload cardiac hypertrophy, they were then fed a high salt (6%NaCl) diet for the next 5 weeks. Data for baseline hypertrophic group (H) was obtained at the end of 11 weeks. Among H group animals, they were divided as follows and treated for an additional 4 weeks: 1) continuation of the HS diet with vehicle injection (H+V); 2) continuation of the HS diet with paricalcitol (19-nor-1,25-(OH)2 D2) (PC) (200ng IP 3x/wk) injection (H+PC); 3) continuation of the HS diet with low dose enalapril (EP), an angiotensin-converting enzyme inhibitor, infusion via osmotic pump and vehicle injection (H+EP+V); and 4) continuation of the HS diet with low dose EP infusion via osmotic pump and PC (200ng IP 3x/wk) injection (H+EP+PC). PC was prepared with 95% propylene glycol and 5% ethyl alcohol solution and administered three times a week on Monday, Wednesday, and Friday for 4 consecutive weeks. Vehicle groups received vehicle injections on the same schedule. Two groups of rats were implanted with pumps to deliver EP for 4 weeks. Since the reduction in blood pressure (BP) from high doses of EP would have effects on cardiac hypertrophy and progression to heart failure, we used low dose EP at 90ug/day, a maximum dose that did not significantly decrease BP in these rats, to study the effects of EP and PC that are independent of BP.
2010-09-14 | E-GEOD-24110 | biostudies-arrayexpress
Project description:Three weeks after infarction, age matched rats with large infarction by ECG criteria were randomly assigned to one of the three groups: 1) Treatment with Captopril for 21 days and a daily subcutaneous dose of DITPA for the last 10 days of treatment, 2) Treatment for 10 days with DITPA alone, 3) Control heart failure and 4) Sham-operated. Keywords: Drug Effects on Heart Failure
2006-07-21 | GSE4963 | GEO
Project description:The goal of this study is to compare the transcriptome of heart failure patients (with ischemic or dilated cardiomyopathy) undergoing heart transplantation compared with healthy controls. We analyzed 36 human samples. 13 from ischemic and 13 from dilated human hearts compared with 10 healthy control donors.
2014-04-28 | E-GEOD-55296 | biostudies-arrayexpress
Project description:Heart failure is a multisystem syndrome caused by structural and functional defects in multiple tissues. The study aims to identify differentially regulated genes in skeletal muscle of heart failure patients. Here, we obtained biopsies from the pectoralis major muscle and performed RNA sequencing to profile the gene expression patterns from six heart failure patients and three healthy controls.
2020-09-07 | E-MTAB-8531 | biostudies-arrayexpress