Single cardiomyocyte nuclear transcriptomes reveal a lincRNA-regulated de-differentiation and cell cycle stress-response in vivo

Kelvin See, Wilson L. W. Tan, Eng How Lim, Zenia Tiang, Li Ting Lee, Peter Y. Q. Li, Tuan D. A. Luu, Matthew Ackers-Johnson and Roger S. Foo ()
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Kelvin See: Genome Institute of Singapore
Wilson L. W. Tan: Genome Institute of Singapore
Eng How Lim: Genome Institute of Singapore
Zenia Tiang: Genome Institute of Singapore
Li Ting Lee: Genome Institute of Singapore
Peter Y. Q. Li: National University Health System, Centre for Translational Medicine
Tuan D. A. Luu: National University Health System, Centre for Translational Medicine
Matthew Ackers-Johnson: National University Health System, Centre for Translational Medicine
Roger S. Foo: Genome Institute of Singapore

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Cardiac regeneration may revolutionize treatment for heart failure but endogenous progenitor-derived cardiomyocytes in the adult mammalian heart are few and pre-existing adult cardiomyocytes divide only at very low rates. Although candidate genes that control cardiomyocyte cell cycle re-entry have been implicated, expression heterogeneity in the cardiomyocyte stress-response has never been explored. Here, we show by single nuclear RNA-sequencing of cardiomyocytes from both mouse and human failing, and non-failing adult hearts that sub-populations of cardiomyocytes upregulate cell cycle activators and inhibitors consequent to the stress-response in vivo. We characterize these subgroups by weighted gene co-expression network analysis and discover long intergenic non-coding RNAs (lincRNA) as key nodal regulators. KD of nodal lincRNAs affects expression levels of genes related to dedifferentiation and cell cycle, within the same gene regulatory network. Our study reveals that sub-populations of adult cardiomyocytes may have a unique endogenous potential for cardiac regeneration in vivo.

Date: 2017
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DOI: 10.1038/s41467-017-00319-8

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