Plasma kynurenine mediated pathological communication between gut microbiota and ventricular remodeling in children with pressure overload
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PROVIDER: PRJNA867689 | ENA |
REPOSITORIES: ENA
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Project description:Abnormally elevated plasma kynurenine (Kyn) was detected in the patient cohort and single nuclues sequecing revealed its molecular role
2023-07-19 | GSE210833 | GEO
Project description:Pathological processes underlying pressure overload triggered heart failure were mainly analyzed from a cardiomyocyte centric view. To identify new cellular mechanisms, we isolated cardiomyocytes, endothelial cells and fibroblasts as most abundant cardiac cell types from mice in the subacute and chronic stages of pressure overload (by transverse aortic constriction, TAC) and performed RNA-sequencing. We detected highly cell-type specific transcriptional responses with characteristic time courses and active intercellular communication, especially early after TAC. We focused on endothelial cells, and single-cell sequencing in this population showed enhanced expression of collagens and inflammatory mediators at this stage. Importantly, these endothelial transcriptional changes were transduced to the translational level as shown by Ribo-Tag sequencing and verification of collagen protein production by cardiac endothelial cells. In conclusion, we provide a resource of cardiac cellular gene expression in pressure overload and reveal the induction of collagens by endothelial cells as potential therapeutic target.
2022-02-08 | GSE180736 | GEO
Project description:Pathological processes underlying pressure overload triggered heart failure were mainly analyzed from a cardiomyocyte centric view. To identify new cellular mechanisms, we isolated cardiomyocytes, endothelial cells and fibroblasts as most abundant cardiac cell types from mice in the subacute and chronic stages of pressure overload (by transverse aortic constriction, TAC) and performed RNA-sequencing. We detected highly cell-type specific transcriptional responses with characteristic time courses and active intercellular communication, especially early after TAC. We focused on endothelial cells, and single-cell sequencing in this population showed enhanced expression of collagens and inflammatory mediators at this stage. Importantly, these endothelial transcriptional changes were transduced to the translational level as shown by Ribo-Tag sequencing and verification of collagen protein production by cardiac endothelial cells. In conclusion, we provide a resource of cardiac cellular gene expression in pressure overload and reveal the induction of collagens by endothelial cells as potential therapeutic target.
2022-02-08 | GSE180733 | GEO
Project description:Pathological processes underlying pressure overload triggered heart failure were mainly analyzed from a cardiomyocyte centric view. To identify new cellular mechanisms, we isolated cardiomyocytes, endothelial cells and fibroblasts as most abundant cardiac cell types from mice in the subacute and chronic stages of pressure overload (by transverse aortic constriction, TAC) and performed RNA-sequencing. We detected highly cell-type specific transcriptional responses with characteristic time courses and active intercellular communication, especially early after TAC. We focused on endothelial cells, and single-cell sequencing in this population showed enhanced expression of collagens and inflammatory mediators at this stage. Importantly, these endothelial transcriptional changes were transduced to the translational level as shown by Ribo-Tag sequencing and verification of collagen protein production by cardiac endothelial cells. In conclusion, we provide a resource of cardiac cellular gene expression in pressure overload and reveal the induction of collagens by endothelial cells as potential therapeutic target.
2022-02-08 | GSE180720 | GEO
Project description:Skeletal muscle derived Musclin protects the heart during pathological overload
| PRJNA530525 | ENA
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
Project description:Pathological cardiac hypertrophy was induced by pressure overload on the heart. We performed genome-wide exon array experiments with left ventricles of mice with 1 week and 4 week of transverse aortic constriction (TAC). The exon level analysis revealed widespread regulation of alternative splicing and alternative polyadenylation during hypertrophy.
2011-05-01 | GSE24242 | GEO
Project description:Pathological cardiac hypertrophy was induced by pressure overload on the heart. We performed genome-wide exon array experiments with left ventricles of mice with 1 week and 4 week of transverse aortic constriction (TAC). The exon level analysis revealed widespread regulation of alternative splicing and alternative polyadenylation during hypertrophy. Exon and gene expression changes were examined in 1 week and 4 week TAC-operated hearts compared to sham-operated hearts. We used C57/BL6 wildtype mice, and their left ventricles were subject to surgery (each n=2).
2011-05-01 | E-GEOD-24242 | biostudies-arrayexpress
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
Project description:Aortic banding is an excellent model system to evaluate the process of development of left ventricular hypertrophy in response to hemodynamic stress. The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different time points after surgical intervention for pressure-overload induced hypertrophy. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/band_home.html Keywords = Pressure overload, cardiac hypertrophy Keywords: time-course
2002-07-30 | GSE76 | GEO