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RNA-seq analysis of diploid and tetraploid neonatal rat cardiomyocytes

ABSTRACT: In response to pathological stress such as congenital heart disease and heart valvular disease, cardiomyocytes (CMs) generally increased the content of DNA and the number of nuclear. This process named CM polyploidization and multi-nucleation, result in the presence of multi-nucleated polyploid CM. However, the significance of multi-nucleated polyploid CM (M*Pc CM) for heart disease remains enigmatic. We speculated that the process of CM polyploidization and multinucleation may be an adaptative response, which may help CM function recovery and survive the stress condition. We sought to determine the mechanism of enhanced mitophagy in M*Pc CMs during hypoxia adaptation.

ORGANISM(S): Rattus rattus

PROVIDER: GSE123322 | GEO | 2021/03/23

REPOSITORIES: GEO

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Project description:The heart is a complex organ composed of multiple cell and tissue types. During early developmental stages, heart cells from different regions of the heart exhibit different patterns of gene expression, which are thought to significantly contribute to heart development and morphogenesis. Until recently, the lack of adequate tools prevented our ability to systematically profile gene expression in a cell type and anatomically-specific manner during heart development. Single cell RNA sequencing has emerged as a powerful approach that allows genome-wide analysis of gene expression in single cells. Using microfluidic-chip and droplet-based single-cell RNA sequencing platforms, we analyze cardiac cells during the early stages of heart development. We found, by principle component analysis, that the expression of cell cycle genes represents a major determinant of transcriptional variation in all analyzed cardiac cell types. Interestingly, when single cardiomyocytes (CMs) from different heart chambers were analyzed, we found that atrial ventricular canal derived CMs have reduced cell cycle activity compare with CMs from the left and right ventricular chambers. In addition, CMs in the trabecular myocardium exhibit reduced cell cycle activity than CMs in the compact myocardium. When CMs within the same chamber were segregated by their cell cycle phase, we found that CMs in the G2/M phase downregulate their sarcomeric and cytoskeletal markers. Finally, we revealed the expression of a signaling ligand from the endocardium that may repress trabecular CM proliferation, and an epicardial-derived ligand that can promote compact CM proliferation. Together these data highlight the variations in cell cycle activity to selectively promote cardiac chamber growth during development and the profound transcriptional shift within the same cell at different phases of cell cycle. Identifying alterations in the expression of key signaling molecules that drive CM proliferation may lead to greater understanding of the onset or progression of congenital heart disease.

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RNA-seq analysis of diploid and tetraploid neonatal rat cardiomyocytes

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