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Transcription profiling of mouse heart samples from pressure overload and sham treated animals from wild type and Apelin knockouts reveals impaired heart function in Apelin

ABSTRACT: The endogenous peptide Apelin is crucial for maintaining heart function in pressure overload and aging Experiment Overall Design: Heart samples from Apelin knockout mice with pressure overload and sham control together with the wild-type mice with pressure overload and sham were compared

ORGANISM(S): Mus musculus

SUBMITTER: Sara Arab

PROVIDER: E-GEOD-7781 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Impaired heart contractility in Apelin gene-deficient mice associated with aging and pressure overload.

Kuba Keiji K Zhang Liyong L Imai Yumiko Y Arab Sara S Chen Manyin M Maekawa Yuichiro Y Leschnik Michael M Leibbrandt Andreas A Markovic Mato M Schwaighofer Julia J Beetz Nadine N Musialek Renata R Neely G Greg GG Komnenovic Vukoslav V Kolm Ursula U Metzler Bernhard B Ricci Romeo R Hara Hiromitsu H Meixner Arabella A Nghiem Mai M Chen Xin X Dawood Fayez F Wong Kit Man KM Sarao Renu R Cukerman Eva E Kimura Akinori A Hein Lutz L Thalhammer Johann J Liu Peter P PP Penninger Josef M JM

Circulation research 20070802 4

Apelin constitutes a novel endogenous peptide system suggested to be involved in a broad range of physiological functions, including cardiovascular function, heart development, control of fluid homeostasis, and obesity. Apelin is also a catalytic substrate for angiotensin-converting enzyme 2, the key severe acute respiratory syndrome receptor. The in vivo physiological role of Apelin is still elusive. Here we report the generation of Apelin gene-targeted mice. Apelin mutant mice are viable and f ...[more]

PMID: 17673668

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Impaired heart function in Apelin gene-deficient mice

Project description:The endogenous peptide Apelin is crucial for maintaining heart function in pressure overload and aging Keywords: knockout

2007-12-25 | GSE7781 | GEO

Identification of differentially expressed genes in mice with chronic heart failure induced by pressure overload

Project description:To investigate the mechanism of chronic heart failure induced by pressure overload, we established an animal model in mice by transverse aortic constriction (TAC), with mice undergoing sham surgery as control.

2023-10-31 | GSE228199 | GEO

Proteomic and Phosphoproteomic Profiling of Heart in Pak2cko Mice Under Pressure Overload

Project description:This study employs a factorial design to delineate the combinatorial effects of cardiac-specific conditional gene knockout and pressure overload-induced cardiac hypertrophy via transverse aortic constriction (TAC). Four experimental cohorts were established: (1) conditional knockout mice subjected to TAC (CKO_TAC), (2) knockout controls with Sham surgery (CKO_Sham), (3) floxed control mice receiving TAC (ff_TAC), and (4) floxed Sham-operated controls (ff_Sham). Following a 5-week pressure overload (TAC), myocardial tissue underwent parallel proteomic and phosphoproteomic profiling using TMT-based quantitative mass spectrometry. This dual-omics approach specifically interrogates: (a) the intrinsic genetic perturbation effect (CKO_ Sham vs ff_ Sham), (b) the pure pressure overload response (ff_TAC vs ff_Sham), and critically, (c) the genotype-by-environment interaction through synergistic/antagonistic divergence between observed versus predicted additive effects in CKO_TAC relative to genetic and surgical controls. Phosphoproteomic data further resolve signaling pathway dynamics underlying phenotypic modulation.

2025-09-25 | PXD067213 | Pride

expression data from Zbtb17 cKO mouse heart after pressure overload

Project description:whole gene expression analysis for ZBTB17 cKO mice after transverse aortic constriction (TAC) We used microarrays to detail the global programme of gene expression underlying hypertrophy and heart failure process upon pressure overload 16 male mice, 4 mice per group, were selected at 8-10 weeks old for 4 weeks of TAC and SHAM and collected samples for RNA extraction and hybridization on Affymetrix microarrays. We included corresponding controls.

2013-09-06 | E-GEOD-50638 | biostudies-arrayexpress

Pressure overload greatly promotes neonatal right ventricular cardiomyocyte proliferation - a new model for heart regeneration study

Project description:Background: Current mammalian model for heart regeneration research is limited in apex amputation or myocardium infarction, both of which are controversy. Moreover, RNAseq demonstrated there were a very limited set of differential expressed genes between sham and operation heart in the myocardium infarction model. Here we investigated whether pressure overload in the right ventricle(RV), a common phenomenon in congenital heart disease children, could be a better animal model for heart regeneration study when consider cardiomyocyte(CM) proliferation as the most important index. Methods and results: Pressure overload was induced by pulmonary artery banding (PAB) on day1 and confirmed by echocardiography and hemodynamic measurements at postnatal day 7(P7). RNAseq analyses of purified RVCM at P7 from PAB and sham-operated rats revealed there were 5469 differential expressed genes between these two groups. GO and KEGG analysis showed that these genes mainly mediated mitosis and cell division. Cell proliferation assay indicates a continuous over-proliferation of RVCM after PAB, in particular for P3. In addition, there were ~2 times-fold increase of Ki67/Phh3 -positive CM in human overload RV compared to non-overload RV. Other features about this model included CM hypotrophy and no fibrosis.. Conclusions: Pressure overload profoundly promotes RVCM proliferation in the neonatal stage both in rats and human beings, activated a regeneration-specific gene program, and may offer a better alternative animal model for heart regeneration research..

2020-08-19 | GSE139561 | GEO

Differential expression of mRNAs in the three stages of heart failure in TAC mice

Project description:To identify the role of mRNA on the mouse heart during pressure overload induced heart failure, we have employed high-throughput sequencing to detect mRNA expression. Samples were collected from the sham group and the pressure overload groups (2, 4 and 8 weeks after TAC), with 2 samples per group. The candidate mRNA that may affect the process of heart failure was screened by comparing the pressure overload groups and the sham group.

2022-03-30 | GSE182985 | GEO

Myocardial gene expression in response to pressure overload

Project description:Myocardial deletion of klf4 sensitizes mouse to pressure overload. In order to gain a better understanding of molecular mechanisms of such alterations, we profiled gene expression before and after 3-day of pressure overload (induced by transverse aortic constriction -TAC) in the hearts from MHC-cre (Cre) control and MHC-cre-klf4-deficient (KO) mice. 10wk old male mice was subjected to transverse aortic constriction (TAC) to induce pressure overload or sham operation as control group. After 3 days, heart was removed and total RNA was extracted from apex and subjected for array analysis. Four animals in each group.

2015-07-01 | E-GEOD-61177 | biostudies-arrayexpress

Differential expression of circRNAs in the three stages of heart failure in TAC mice

Project description:To identify the role of circRNA on the mouse heart during pressure overload induced heart failure, we have employed circRNA microarray expression profiling as a discovery platform to detect circRNA expression. Samples were collected from the sham group and the pressure overload groups (2, 4 and 8 weeks after TAC), with 2 samples per group. The candidate circRNA that may affect the process of heart failure was screened by comparing the pressure overload groups and the sham group.

2022-03-30 | GSE182912 | GEO

Dynamic adaptation of myocardial proteome during heart failure development after induction of left ventricular pressure overload in mice

Project description:We analyzed time dependent global proteomic adaptations during heart failure (HF) progression in a mouse model, suffering from left ventricular pressure overload due to transverse aortic constriction (TAC), to gain deeper insights in the disease development and identify new biomarker candidates. The hearts from TAC and sham mice were examined by cardiac MRI on either day 4, 14, 21, 28, 42, and 56 after surgery (n=6 group/time point). At each time point, proteomes of the left (LV) and right ventricles (RV) of TAC and sham mice were analyzed by mass spectrometry (MS).

2018-07-16 | PXD007171 | Pride

Transcription profiling of mouse model of pressure overload

Project description:Pressure overload (PO) leads first to cardiac hypertrophy and later to heart failure. In mice, PO leads to sex differences in cardiac morphology and function. However, early sex differences in gene regulation that precede sex differences in function have not yet been identified. To identify such changes, we developed a model of PO that is characterized by compensated hypertrophy without sex differences after 2 weeks and by heart failure with sex differences after 9 weeks. We used transverse aortic constriction (TAC) or sham-operation in male and female mice and analyzed gene expression by microarray experiments. Experiment Overall Design: The gene expression induced by pressure overload in female and male mice in comparison to sham operated control mice was investigated. For each of these four conditions four biological replicates were performed and the individual samples were hybridized seperately on Affymetrix RAE 430A GeneChip Arrays.

2008-06-15 | E-GEOD-6970 | biostudies-arrayexpress

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