The cells, studied in young zebrafish, moved from the atrium to the ventricle when the ventricle was injured in the study. These cells then spontaneously changed from atrial cardiomyocytes into ventricular cardiomyocytes. The damaged ventricles regained nearly all their function.
The study was published in the June 19 issue of Nature. Neil Chi, an assistant professor of medicine of cardiology at UCSD, was the senior author. Ruilin Zhang, a UCSD postdoc, was the first author.
Humans may have a similar kind of cell usable for treating heart failure patients, the study stated.
"Although it remains to be elucidated whether mammalian atrial cardiomyocytes may also have a comparable transdifferentiation capacity, recent studies have indicated that mammalian cardiomyocyte progenitor cells (CPMCs) appear to be enriched in the atrium, suggesting that the zebrafish transdifferentiating atrial cardiomyocytes may be analogous to the atrial-resident adult CPMCs," the study said.
Zebrafish ventricular cardiomyoctes were selectively destroyed by transgenically attaching a bacterial protein to the cells along with the mCherry red fluorescent protein, then administering the antibiotic metronidazole.
This combination allowed the cell types to be visually tracked before and after the ventricle was damaged. After the injury, green-tagged atrial cardiomyocytes could be spotted in the ventricle, repairing its function.
"We observed that Notch signalling becomes activated in the atrial endocardium following ventricular
ablation, and discovered that inhibiting Notch signalling blocked the atrial-to-ventricular transdifferentiation and cardiac regeneration," the study stated. "Overall, these studies not only provide evidence for the plasticity of cardiac lineages during myocardial injury, but more importantly reveal an abundant new potential cardiac resident cellular source for cardiac ventricular regeneration."
Other contributors to the paper include, Peidong Han, Hongbo Yang, Kunfu Ouyang, Derek Lee, Ju Chen,Yi-Fan Lin and Deborah Yelon, UCSD; Karen Ocorr, Sanford-Burnham Institute for Medical Research; Guson Kang and Didier Y. R. Stainier, UCSF.