Data from: Single-cell Transcriptome and Epigenomic Reprogramming of Cardiomyocyte-Derived Cardiac Progenitor Cells

The molecular basis underlying spontaneous dedifferentiation and cell cycle reentry of mammalian adult cardiomyocytes (ACMs) during cardiac tissue regeneration is poorly understood. We present data integrating single-cell transcriptome and whole-genome DNA methylome analyses of mouse ACMs to better understand the epigenomic signatures governing their intrinsic cellular plasticity. Compared to parental cardiomyocytes, dedifferentiated myocyte-derived cardiac progenitor-like cells (mCPCs) display epigenomic reprogramming with many differentially-methylated regions, both hypermethylated and hypomethylated, across the entire genome. Correlating well with the methylome, our transcriptomic array data derived from single-cell microfluidics show that the genes encoding cardiac structure and function proteins are remarkably down-regulated in mCPCs, while those for cell cycle, proliferation, and stemness are significantly up-regulated. This dataset suggests that the cellular plasticity of mammalian cardiomyocytes is the result of a well-orchestrated epigenomic reprogramming and a subsequent global transcriptomic alteration. Understanding how to reprogram cardiomyocyte epigenomic signatures may enable the design of future clinical therapies that induce cardiac regeneration, and prevent heart failure.