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Differential regulation of extracellular matrix constituents in myocardial remodeling with and without heart failure following pressure overload

ABSTRACT: The aim of the present study was to examine potential differences in the regulation of myocardial ECM constituents, in mice that develop hypertrophy only (ABnonHF) and in mice that develop overt heart failure (ABHF) as response to pressure overload. Seven weeks old male C57BL/6 mice were subjected to aortic banding (AB) or sham operation (sAB), with sacrifice 4 weeks after banding. Prior to sacrifice, cardiac function and geometry were evaluated by echocardiography. Animals with comparable gradients over the banded ascending aorta, comparable cardiac output and heart rate were divided into two groups: ABnonHF and ABHF. Our criterion for dividing AB animals into these two groups was based on lung weight and left atrial diameter (LAD), as an increase in these parameters most likely is due to pulmonary congestion. Heart failure (HF) was defined as an increase in lung weight and LAD defining ABnonHF as lung weight/tibia length ≤ 10.5 mg/mm and LAD ≤ 2.0 mm and ABHF as lung weight/tibia length ≥ 15 mg/mm and LAD ≥ 2.4 mm.

ORGANISM(S): Mus musculus

PROVIDER: GSE36074 | GEO | 2012/11/01

SECONDARY ACCESSION(S): PRJNA151837

REPOSITORIES: GEO

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Differential regulation of extracellular matrix constituents in compensated versus decompensated heart failure following pressure overload

Project description:The aim of the present study was to examine potential differences in the regulation of myocardial ECM constituents, in mice that develop hypertrophy only (ABnonHF) and in mice that develop overt heart failure (ABHF) as response to pressure overload. Seven weeks old male C57BL/6 mice were subjected to aortic banding (AB) or sham operation (sAB), with sacrifice 4 weeks after banding. Prior to sacrifice, cardiac function and geometry were evaluated by echocardiography. Animals with comparable gradients over the banded ascending aorta, comparable cardiac output and heart rate were divided into two groups: ABnonHF and ABHF. Our criterion for dividing AB animals into these two groups was based on lung weight and left atrial diameter (LAD), as an increase in these parameters most likely is due to pulmonary congestion. Heart failure (HF) was defined as an increase in lung weight and LAD defining ABnonHF as lung weight/tibia length M-bM-^IM-$ 10.5 mg/mm and LAD M-bM-^IM-$ 2.0 mm and ABHF as lung weight/tibia length M-bM-^IM-% 15 mg/mm and LAD M-bM-^IM-% 2.4 mm. Microarray screening was performed in 7 mice from each AB group and in 5 sAB mice. Sham was used as control.

2012-11-01 | E-GEOD-36074 | biostudies-arrayexpress

Expression data from mouse heart after aortic binding surgery for 2 weeks

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2020-03-04 | GSE96038 | GEO

High expression genes in urethane-induced lung tumor

Project description:We estimated differences of urethane-induced tumors between Nrf2+/+ and Nrf2-/- ICR mouse. To identify Nrf2-regulated genes in tumors, we examined the mRNA expression profile both in tumor and non-tumor tissue of mouse 4 months after urethane administration. We performed microarray analyses using the comparable size of lung tumors (1.0 mm < tumor diameter < 1.5 mm) and intact non-tumor lung tissues derived either from Nrf2+/+ (n=8) or Nrf2–/–mice (n=8) at 16-weeks after urethane(1-g/kg body weight) treatment.

2013-04-16 | E-GEOD-46048 | biostudies-arrayexpress

Reverse myocardial remodeling by aortic bending debanding in mice

Project description:The objective of this study was to identify alterations in gene expression during reverse myocardial remodeling in a mouse model of reversible pressure overload. Mice were subjected to 4 weeks of aortic banding (AB) or sham procedure (sAB), banding and subsequent debanding (DB3), or sham procedure and subsequent debanding (sDB3), with saccrifice 3 days after debanding.

2010-09-30 | GSE24454 | GEO

Transcription profiling of mouse treated by ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium reveals CHF1/Hey2 promotes physiological hypertrophy in response to pressure overload

Project description:We have previously found that overexpression of CHF1/Hey2 in the myocardium prevents the development of phenylephrine-induced hypertrophy. To determine the role of CHF1/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild type and transgenic mice overexpressing CHF1/Hey2 in the myocardium. We found that both wild type and transgenic mice developed increased ventricular weight to body weight ratios one week after aortic banding. Wild type mice also developed decreased fractional shortening after one week when compared to preoperative echocardiograms and sham operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild type cells. Gene Set Analysis of microarray data from wild type and transgenic hearts one week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling and biosynthesis. These findings demonstrate that CHF1/Hey2 promotes physiological over pathological hypertrophy in pressure overload through suppression of apoptosis and global regulation of multiple transcriptional pathways. Experiment Overall Design: Ascending aortic banding on four wild type and four transgenic mice were compared

2010-02-17 | E-GEOD-13031 | biostudies-arrayexpress

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2009-06-16 | E-GEOD-16624 | biostudies-arrayexpress

Rat LAD IR study

Project description:Rats underwent surgery for LAD ligation for 30 min followed by reperfusion. Heart ventricles were collected 2d or 7d after reperfusion. Keywords: rat heart ventricles, LAD - left anterior descending coronary artery, IR - ischemia-reperfusion

2006-03-24 | GSE4105 | GEO

Reduced heart failure effects through novel integrin targeting approach

Project description:Heart failure remains one of the largest clinical burdens globally, with little to no improvement in the development of disease-eradicating therapeutics. Integrin targeting has been used in the treatment of ocular disease and cancer, but little is known about its utility in the treatment of heart failure. Here we sought to determine whether the second generation orally available, αvβ3-specific RGD-mimetic, 29P, was cardioprotective. Male mice were subjected to transverse aortic constriction (TAC) and treated with 50μg/kg 29P or volume-matched saline as Vehicle control. At 3 weeks post-TAC, echocardiography showed that 29P treatment significantly restored cardiac function and structure indicating the protective effect of 29P treatment in this model of heart failure. Importantly, 29P treatment improved cardiac function giving improved fractional shortening, ejection fraction, heart weight and lung weight to tibia length fractions, together with partial restoration of Ace and Mme levels, as markers of the TAC insult. At a tissue level, 29P reduced cardiomyocyte hypertrophy and interstitial fibrosis, both of which are major clinical features of heart failure. RNA sequencing identified that, mechanistically, this occurred with concomitant alterations to genes involved molecular pathways associated with these processes such as metabolism, hypertrophy and basement membrane formation. Overall, targeting αvβ3 with 29P provides a novel strategy to attenuate pressure-overload induced cardiac hypertrophy and fibrosis, providing a possible new approach to heart failure treatment.

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Pulmonary artery banded rat heart

Project description:Changes in juvenile rat heart with pulmonary artery banding

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