| First Author | Hatzistergos KE | Year | 2020 |
| Journal | Sci Adv | Volume | 6 |
| Issue | 49 | PubMed ID | 33268364 |
| Mgi Jnum | J:349587 | Mgi Id | MGI:6727606 |
| Doi | 10.1126/sciadv.aba9950 | Citation | Hatzistergos KE, et al. (2020) A novel cardiomyogenic role for Isl1(+) neural crest cells in the inflow tract. Sci Adv 6(49) |
| abstractText | The degree to which populations of cardiac progenitors (CPCs) persist in the postnatal heart remains a controversial issue in cardiobiology. To address this question, we conducted a spatiotemporally resolved analysis of CPC deployment dynamics, tracking cells expressing the pan-CPC gene Isl1 Most CPCs undergo programmed silencing during early cardiogenesis through proteasome-mediated and PRC2 (Polycomb group repressive complex 2)-mediated Isl1 repression, selectively in the outflow tract. A notable exception is a domain of cardiac neural crest cells (CNCs) in the inflow tract. These "dorsal CNCs" are regulated through a Wnt/beta-catenin/Isl1 feedback loop and generate a limited number of trabecular cardiomyocytes that undergo multiple clonal divisions during compaction, to eventually produce ~10% of the biventricular myocardium. After birth, CNCs continue to generate cardiomyocytes that, however, exhibit diminished clonal amplification dynamics. Thus, although the postnatal heart sustains cardiomyocyte-producing CNCs, their regenerative potential is likely diminished by the loss of trabeculation-like proliferative properties. |
