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Transcriptomic and Functional Analyses of Mitochondrial Dysfunction in Pressure Overload-induced Right Ventricular Failure

ABSTRACT: Transcriptomic and Functional Analyses of Mitochondrial Dysfunction in Pressure Overload-induced Right Ventricular Failure

PROVIDER: PRJNA639270 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12007708.fastq.gz	Fastqsanger.gz
	SRR12007709.fastq.gz	Fastqsanger.gz
	SRR12007710.fastq.gz	Fastqsanger.gz
	SRR12007711.fastq.gz	Fastqsanger.gz
	SRR12007712.fastq.gz	Fastqsanger.gz

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Transcriptomic and Functional Analyses of Mitochondrial Dysfunction in Pressure Overload-induced Right Ventricular Failure

Project description:Background: In complex congenital heart disease patients such as those with tetralogy of Fallot, the right ventricle (RV) is subject to pressure overload, leading to RV hypertrophy and eventually RV failure. The mechanisms that promote the transition from stable RV hypertrophy to RV failure are unknown. We evaluated the role of mitochondrial bioenergetics in the development of RV failure. Methods: We created a murine model of RV pressure overload by pulmonary artery banding and compared with sham-operated controls. Gene expression by RNA-sequencing, oxidative stress, mitochondrial respiration, dynamics, and structure were assessed in pressure overload-induced RV failure. Results: RV failure was characterized by decreased expression of electron transport chain genes and mitochondrial antioxidant genes (aldehyde dehydrogenase 2 and superoxide dismutase 2) and increased expression of oxidant stress markers (heme oxygenase, 4-hydroxynonenal). The activities of all electron transport chain complexes decreased with RV hypertrophy and further with RV failure (oxidative phosphorylation: sham 552.3±43.07 vs. RV hypertrophy 334.3±30.65 vs. RV failure 165.4±36.72 pmol/(sec*ml), p<0.0001). Mitochondrial fission protein DRP1 did not change, while MFF decreased and fusion protein OPA1 decreased. In contrast, transcription of electron transport chain genes increased in the left ventricle of RV failure. Conclusion: Pressure overload-induced RV failure is characterized by decreased transcription and activity of electron transport chain complexes and increased oxidative stress which are associated with decreased energy generation. An improved understanding of the complex processes of energy generation could aid in developing novel therapies to mitigate mitochondrial dysfunction and delay the onset of RV failure.

2021-03-18 | GSE152413 | GEO

Right ventricular failure due to coronary artery ligation

Project description:A porcine microarray study of acute right ventricular failure due to coronary artery ligation of the right ventricular free wall. 1. Baseline sample from the free right ventricular wall. 2. Ligation of the coronary arteries on the right ventricular free wall induced right ventricular heart failure. When the pressure in the right atrium rose to >20 mmHg, heart failure samples were taken from the free right ventricular wall.

2011-08-24 | GSE31619 | 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

Right ventricular failure due to pulmonary banding

Project description:Right ventricular failure was induced thourgh pulmonary banding in 11 pigs. Right ventricular failure was defined as a SRVP >50 mmHg during two hours. After right ventricular failure was induced, half the pigs were treatmed with a Glenn-shunt combined with pulmonary banding for one hour, and the other half served as control group with pulmonary banding only. The aim was to study the change in global gene expression during right ventricular failure due to pulmonary banding, and the effect of volume unloading during pulmonary banding. 11 pigs. Samples at the following time periods: 1) Baseline 2) Right ventricular failure 3) Treatment with modified Glenn-shunt/Control. After Right ventricular failure, pigs were divided into two groups a) Treatment with modified Glenn-shunt or b) Control group

2013-06-11 | E-GEOD-47814 | biostudies-arrayexpress

Development of Specific Therapy Against Right Ventricular Failure

Project description:Right ventricular (RV) failure plays a critical role in any type of heart failure. However, there is no specific therapy developed for RV failure. To understand RV failure, we focused on the RV specific genes. Global gene expression analysis showed that alternative complement pathway-related genes including C3 and Cfd were significantly upregulated in right ventricle in murine heart. We generated the RV failure by right ventricle-specific pressure overload model mice, pulmonary artery constriction (PAC), which induces RV failure around 14 days. In C3 knockout (C3KO) mice, PAC-induced RV dysfunction and fibrosis were significantly attenuated. C3a is produced from C3 by C3 convertase complex including Cfd. Cfd knockout mice also attenuated PAC-induced RV failure. Moreover, C3a receptor (C3aR) antagonist dramatically improved PAC-induced RV dysfunction in wild type mice. Here we revealed the crucial role of C3-Cfd-C3a-C3aR axis in RV failure and highlight the potential therapeutic target for RV failure with no pharmacologic option.

2021-09-07 | GSE183504 | GEO

Development of Specific Therapy Against Right Ventricular Failure (in vitro analysis)

Project description:Right ventricular (RV) failure plays a critical role in any type of heart failure. However, there is no specific therapy developed for RV failure. To understand RV failure, we focused on the RV specific genes. Global gene expression analysis showed that alternative complement pathway-related genes including C3 and Cfd were significantly upregulated in right ventricle in murine heart. We generated the RV failure by right ventricle-specific pressure overload model mice, pulmonary artery constriction (PAC), which induces RV failure around 14 days. After administration of C3a receptor (C3aR) antagonist, RV function was dramatically improved PAC-induced RV dysfunction in wild type mice. To investigate the role of C3a to cardiomyocyte, C3a recombinant protein was administerd to neonatal rat ventricular myocytes (NRVMs), the results that several MAP kinesis were phosphorylated by C3a. In turn, to identify the key expressed genes as downstream of C3a in NRVMs, global gene expression analysis was performed in vitro.

2021-09-07 | GSE183503 | GEO

Right ventricular failure due to pulmonary banding

2013-06-11 | GSE47814 | GEO

Effect of neonatal right ventricular pressure overload on gene expression and regions of open chromatin during postnatal heart development

Project description:To investigate the effect of pressure overload (PO) during postnatal right ventricular (RV) development, we established the RV PO model by conducting pulmonary artery banding (PAB) surgery on neonatal Sprague-Dawley (SD) rats. We then performed gene expression and chromatin openness profiling analysis using data obtained from RNA-seq and ATAC-seq of RV free walls from PO and sham-operated rats at postnatal day 21 (P21).

2024-05-17 | GSE210180 | GEO

Chemokines regulate small leucine-rich proteoglycans in the extracellular matrix of the pressure-overloaded right ventricle

Project description:Chemokines have been suggested to play a role during development of left ventricular failure, but little is known about their role during right ventricular (RV) remodeling and dysfunction. The first aim of this study was to identify chemokines which are regulated during RV pressure overload. We then hypothesized that these chemokines regulate SLRPs (small leucine-rich proteoglycans) A microarray study was performed on 5 pulmonary banded and sham operated wildype mice.

2011-08-09 | E-GEOD-30922 | biostudies-arrayexpress

Chemokines regulate small leucine-rich proteoglycans in the extracellular matrix of the pressure-overloaded right ventricle

2011-08-10 | GSE30922 | GEO