A recent study from Mariko Omatsu-Kanbe, Yuka Nishino and Nozomi Nozuchi,etc. shows that prion protein- and cardiac troponin T-marked interstitial cells from the adult myocardium  spontaneously develop into beating cardiomyocytes.

Evidence from their research showing that the number of beating ACMs reaches a plateau in adulthood in the postnatal mouse heart and that PrP⁺cTnT⁺ cells are detected in human heart tissues derived from patients over 80 years of age suggests that native ACMs stay in the heart until advanced stages, without appreciably differentiating into normal cardiomyocytes, under physiological conditions. They usually counted ~500 beating ACMs per heart after several days of culture, which is thought to be lower than the actual number of ACMs resident in the heart. This underestimation of the cell number may due to the loss of a number of native ACMs following repeated centrifugation during the isolation procedure, as the isolated ventricular fraction contains heterogeneous small cells, including native ACMs, co-precipitated with cardiomyocytes, and/or to the reduced ability to develop into beating cells during the preparation procedures.

It is expected that the quiescence of native ACMs under physiological conditions makes it possible for these cells to stay within the normal heart highly organized to generate rhythmic impulses to induce rhythmic contractions of cardiomyocytes. On the other hand, ACMs preserve their ability to develop into beating cells under culture conditions, even immature and incomplete cardiomyocytes. It may therefore be possible in the future to identify certain culture conditions to develop native ACMs into more mature cardiomyocytes following the complete isolation of these cells.

The trigger of starting the spontaneous development of native ACMs into beating cells remains unclear, at least with respect to the isolation of the cells and culture under three-dimensional conditions using methylcellulose-based semisolid culture medium. In the present and previous studies, they found that sufficient isolation of native ACMs from neighboring ventricular myocytes is required to yield beating cells in culture, and, indeed, insufficient enzymatic digestion results in the failure to obtain beating ACMs from the mouse heart. In the normal mouse or human heart, PrP⁺cTnT⁺ native ACMs were usually observed as solitary or clustered cells, but not multinucleated cells. These observations also suggest that the fusion or multinucleation of ACMs occurs after the isolation procedures. These data may lead to the view that the independence of native ACMs from the microenvironments due to the death of the neighboring ventricular myocytes stimulates the spontaneous development of these cells into beating cardiomyocytes under pathophysiological conditions. It would be of interest to explore the nature of ACMs in infarct areas and/or border zones in which adjacent cardiomyocytes die in diseased human hearts in the future study.

Their findings are thus considered to provide a view concerning the presence of quiescent but still functionally viable cells in the normal adult organ that originate from the fetal stage tissues.

Reference

Prion protein- and cardiac troponin T-marked interstitial cells from the adult myocardium spontaneously develop into beating cardiomyocytes, Scientific Reports 4,Article number: 730︱doi:10.1038/srep07301