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Cardiac transcriptome analysis of right and left ventricular heart specimens of BBLN-transgenic mice by NGS

ABSTRACT: The study performed NGS to investigate the cardiac transcriptomes of right and left ventricular heart specimens of 3-4-month-old BBLN-transgenic mice with FVB/N background in comparison to those of non-transgenic FVB/N mice. BBLN-transgenic (Tg-BBLN) mice with myocardium-specific BBLN expression were generated to investigate the cardiac phenotype of increased cardiac BBLN transcript levels because the function of BBLN (Bublin coiled-coil protein), which is the chromosome 9 open reading frame(C9orf16), is largely unknown. Tg-BBLN mice with increased cardiac BBLN levels developed features of heart failure with increasing age. Pathomechanisms of heart failure induced by BBLN were investigated by NGS of right and left ventricular heart specimens of male, BBLN-transgenic mice (age: 3-4 months). NGS data reveal transcriptome changes in right and left ventricular heart specimens induced by increased expression of BBLN in the heart.

ORGANISM(S): Mus musculus

PROVIDER: GSE241022 | GEO | 2023/09/18

REPOSITORIES: GEO

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Cardiac transcriptome analysis of BBLN-transgenic mice by NGS

Project description:The study applied NGS to determine the cardiac transcriptomes of BBLN-transgenic mice with FVB/N background in comparison to those of non-transgenic FVB/N mice at an age of 8 months. The BBLN (Bublin coiled-coil protein) is the chromosome 9 open reading frame, C9orf16, with largely unknown function. To investigate the cardiac phenotype of increased cardiac BBLN transcript levels we generated BBLN-transgenic (Tg-BBLN) mice. Echocardiography documented that Tg-BBLN mice developed features of heart failure at an age of 8 months. To elucidate pathomechanisms of heart failure induced by BBLN, we performed NGS of the cardiac transcriptomes of eight-month-old, male, BBLN-transgenic mice with cardiac-specific expression of BBLN under control of the myocardium-specific, alpha-MHC promoter. The non-transgenic control group are age-matched, male, nontransgenic FVB/N mice. NGS data of this study document transcriptome changes underlying the heart failure phenotype induced by transgenic BBLN expression.

2023-09-18 | GSE241161 | GEO

Whole genome microarray gene expression profiling of transgenic mouse hearts with four-fold increased BBLN contents

Project description:The study performed whole genome microarray gene expression profiling of mouse hearts from BBLN-transgenic mice with four-fold increased cardiac BBLN (Bublin coiled coil protein) contents (Tg-BBLN-low) in comparison to non-transgenic FVB hearts. Tg-BBLN-low mice with four-fold increased cardiac BBLN expression under control of the myocardium-specific alpha-MHC promoter developed features of compensated heart failure with increasing age, which was characterized by a significantly reduced left ventricular ejection fraction as determined by echocardiography. To investigate the compensated heart failure phenotype of Tg-BBLN-low mice, whole genome micoarray gene expression profiling was performed. The microarray data show that moderately increased cardiac BBLN levels are sufficient to induce features of pathological cardiac remodeling.

2023-09-18 | GSE241030 | 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

Whole genome microarray gene expression profiling of right ventricular heart specimens from pediatric patients with Tetralogy of Fallot (TOF)

Project description:Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart defect with a world-wide prevalence of 3 to 4 cases per 10,000 life births. TOF is a congenital heart disease with four major cardiac defects, i.e., ventricular septal defect, overriding aortic root, infundibular stenosis of the pulmonary artery, and right ventricular hypertrophy. Treatment relies on correction surgery in early infancy. This study performed whole genome microarray gene expression profiling of cardiac specimens of the right ventricular outflow tract (RVOT), which were recovered during correction surgery of TOF from 11 pediatric patients diagnosed with TOF cardiac defects.

2023-09-18 | GSE241024 | GEO

Cardiac transcriptome analysis of RKIP-transgenic and GRK2-transgenic mice by NGS

Project description:The RAF kinase inhibitor protein, RKIP, is a dual inhibitor of the RAF1 kinase and the G-protein-coupled receptor kinase 2 (GRK2). By inhibition of the proto-oncogenic and pro-survival RAF1-MAPK pathway, the RAF kinase inhibitor protein, RKIP, acts as a tumor suppressor, which enhances cardiomyocyte death and promotes the development of symptoms of heart failure. To elucidate pathomechanisms of heart failure induced by RKIP, the study determined the cardiac transcriptomes of eight-month-old, male, transgenic mice with cardiac-specific expression of RKIP (PEBP1) under control of the myocardium-specific, alpha-MHC promoter. In addition, the study determined the cardiac transcriptomes of GRK2-transgenic mice. Tg-GRK2 mice have a slightly increased transgenic expression of GRK2. According to NGS data, cardiac GRK2-Grk2 transcript levels of Tg-GRK2 mice are 1.59±0.10-fold higher than those of non-transgenic FVB hearts. In Tg-GRK2 mice, transgenic GRK2 is expressed under control of the ubiquitous CMV immediate-early promoter/enhancer. The non-transgenic control group are age-matched, male, nontransgenic FVB/N mice. NGS data of this study document transcriptome changes underlying the heart failure phenotype induced by transgenic RKIP expression and cardiac degeneration induced by GRK2 expression.

2021-12-27 | GSE191316 | GEO

Spatially resolved multiomics of human cardiac niches - Visium

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2023-06-01 | E-MTAB-12975 | biostudies-arrayexpress

Spatially resolved multiomics of human cardiac niches - Multiome GEX

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2023-06-13 | E-MTAB-12919 | biostudies-arrayexpress

Heart ventricles proteomic profile in pulmonary arterial hypertension

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

Cardiac perilipin 5 promotes physiological cardioprotective hypertrophy through increased calcium handling and cardiomyocyte contractility

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

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