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Single-cell RNA sequencing reveals the impact of CD34+ cells during heart failure in the hypertrophic heart with hyperlipidemia

ABSTRACT: Hyperlipidemia and hypertension might play a role in cardiac fibrosis, in which a heterogeneous population of fibroblasts seems important. However, it is unknown whether CD34+ cells are involved in the pathogenesis of cardiac fibrosis. This study aimed to investigate the mechanism of CD34+ cell differentiation in cardiac fibrosis during hyperlipidemia. By analyzing the transcriptomes of single cells from the Cd34-CreERT2;R26-tdTomato&ApoE-/- heart, we also demonstrated the dynamics of cell landscape during cardiac fibrosis in the hypertrophic heart with hyperlipidemia.

ORGANISM(S): Mus musculus

PROVIDER: GSE243389 | GEO | 2024/08/17

REPOSITORIES: GEO

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Single-cell RNA sequencing reveals the impact of CD34+ cells in heart failure

Project description:CD34+ cells have been used to treat the patients with heart failure, but the outcome is variable. It is of great significance to scrutinize the fate and the mechanism of CD34+ cell differentiation in vivo during heart failure and explore its intervention strategy. By analyzing the transcriptomes of single cells from the Cd34-CreERT2;R26-tdTomato heart, we illustrated the dynamics of cell landscape during the progression of heart hypertrophy, including CD34+ cells, fibroblasts, endothelial cells and immune cells. And Our study also provides a cellular landscape of CD34+ cell-derived cells in the hypertrophy heart of animal models.

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Single-cell RNA sequencing reveals the impact of CD34+ cells during heart failure in the hypertrophic heart with hyperlipidemia

Project description:Single-cell RNA sequencing reveals the impact of CD34+ cells during heart failure in the hypertrophic heart with hyperlipidemia

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Transcription profiling of hearts from mice heterozygous for Gata4 mutation (G4D) to investigate the significance of Gata4 in regulating postnatal heart function and in regulating the hypertrophic response of the heart to pathological stress.

Project description:An important event in the pathogenesis of heart failure is the development of pathological cardiac hypertrophy. In cultured cardiac cardiomyocytes, the transcription factor Gata4 is required for agonist-induced cardiomyocyte hypertrophy. We hypothesized that in the intact organism Gata4 is an important regulator of postnatal heart function and of the hypertrophic response of the heart to pathological stress. To test this hypothesis, we studied mice heterozygous for deletion of the second exon of Gata4 (G4D). At baseline, G4D mice had mild systolic and diastolic dysfunction associated with reduced heart weight and decreased cardiomyocyte number. After transverse aortic constriction (TAC), G4D mice developed overt heart failure and eccentric cardiac hypertrophy, associated with significantly increased fibrosis and cardiomyocyte apoptosis. Inhibition of apoptosis by overexpression of the insulin-like growth factor 1 receptor prevented TAC-induced heart failure in G4D mice. Unlike WT-TAC controls, G4D-TAC cardiomyocytes hypertrophied by increasing in length more than width. Gene expression profiling revealed upregulation of genes associated with apoptosis and fibrosis, including members of the TGF? pathway. Our data demonstrate that Gata4 is essential for cardiac function in the postnatal heart. After pressure overload, Gata4 regulates the pattern of cardiomyocyte hypertrophy and protects the heart from load-induced failure. Experiment Overall Design: We reasoned that if Gata4 was a crucial regulator of pathways necessary for cardiac hypertrophy, then modest reductions of Gata4 activity should result in an observable cardiac phenotype. To test this hypothesis, we used gene targeted mice that express reduced levels of Gata4. We characterized these mice at baseline and after pressure Experiment Overall Design: overload.

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