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Analysis of cardiomyocyte clonal expansion during mouse heart development and injury.
- Source :
-
Nature communications [Nat Commun] 2018 Feb 21; Vol. 9 (1), pp. 754. Date of Electronic Publication: 2018 Feb 21. - Publication Year :
- 2018
-
Abstract
- The cellular mechanisms driving cardiac tissue formation remain poorly understood, largely due to the structural and functional complexity of the heart. It is unclear whether newly generated myocytes originate from cardiac stem/progenitor cells or from pre-existing cardiomyocytes that re-enter the cell cycle. Here, we identify the source of new cardiomyocytes during mouse development and after injury. Our findings suggest that cardiac progenitors maintain proliferative potential and are the main source of cardiomyocytes during development; however, the onset of αMHC expression leads to reduced cycling capacity. Single-cell RNA sequencing reveals a proliferative, "progenitor-like" population abundant in early embryonic stages that decreases to minimal levels postnatally. Furthermore, cardiac injury by ligation of the left anterior descending artery was found to activate cardiomyocyte proliferation in neonatal but not adult mice. Our data suggest that clonal dominance of differentiating progenitors mediates cardiac development, while a distinct subpopulation of cardiomyocytes may have the potential for limited proliferation during late embryonic development and shortly after birth.
- Subjects :
- Animals
Animals, Newborn
Cell Differentiation
Cell Lineage
Cell Proliferation
Embryonic Stem Cells cytology
Female
Fetal Heart cytology
Fetal Heart growth & development
Heart Injuries genetics
Male
Mice
Mice, Transgenic
Myoblasts, Cardiac cytology
Myocardial Infarction genetics
Myocardial Infarction pathology
Myocytes, Cardiac metabolism
Pericardium cytology
Pericardium embryology
Pericardium growth & development
Pregnancy
Sequence Analysis, RNA
Heart growth & development
Heart Injuries pathology
Myocytes, Cardiac cytology
Subjects
Details
- Language :
- English
- ISSN :
- 2041-1723
- Volume :
- 9
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Nature communications
- Publication Type :
- Academic Journal
- Accession number :
- 29467410
- Full Text :
- https://doi.org/10.1038/s41467-018-02891-z