Abstract:
:Zebrafish heart regeneration occurs through the activation of cardiomyocyte proliferation in areas of trauma. Here, we show that within 3 hr of ventricular injury, the entire endocardium undergoes morphological changes and induces expression of the retinoic acid (RA)-synthesizing enzyme raldh2. By one day posttrauma, raldh2 expression becomes localized to endocardial cells at the injury site, an area that is supplemented with raldh2-expressing epicardial cells as cardiogenesis begins. Induced transgenic inhibition of RA receptors or expression of an RA-degrading enzyme blocked regenerative cardiomyocyte proliferation. Injured hearts of the ancient fish Polypterus senegalus also induced and maintained robust endocardial and epicardial raldh2 expression coincident with cardiomyocyte proliferation, whereas poorly regenerative infarcted murine hearts did not. Our findings reveal that the endocardium is a dynamic, injury-responsive source of RA in zebrafish, and indicate key roles for endocardial and epicardial cells in targeting RA synthesis to damaged heart tissue and promoting cardiomyocyte proliferation.
journal_name
Dev Celljournal_title
Developmental cellauthors
Kikuchi K,Holdway JE,Major RJ,Blum N,Dahn RD,Begemann G,Poss KDdoi
10.1016/j.devcel.2011.01.010subject
Has Abstractpub_date
2011-03-15 00:00:00pages
397-404issue
3eissn
1534-5807issn
1878-1551pii
S1534-5807(11)00038-4journal_volume
20pub_type
杂志文章abstract::Manipulation of cellular identity in the laboratory is generally inefficient due to stochastic events, including epigenomic alterations. Recently in Science, Zuryn et al. (2014) demonstrate that the efficiency of a naturally occurring transdifferentiation event in Caenorhabditis elegans is ensured through stepwise epi...
journal_title:Developmental cell
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