Transient reprogramming of postnatal cardiomyocytes to a dedifferentiated stateCitation formats

  • External authors:
  • Thomas Kisby
  • Irene De Lázaro
  • Maria Stylianou
  • Atsushi Asakura (Editor)

Standard

Transient reprogramming of postnatal cardiomyocytes to a dedifferentiated state. / Kisby, Thomas; De Lázaro, Irene; Stylianou, Maria; Cossu, Giulio; Kostarelos, Kostas; Asakura, Atsushi (Editor).

In: PLoS ONE, Vol. 16, No. 5, e0251054, 05.05.2021.

Research output: Contribution to journalArticlepeer-review

Harvard

Kisby, T, De Lázaro, I, Stylianou, M, Cossu, G, Kostarelos, K & Asakura, A (ed.) 2021, 'Transient reprogramming of postnatal cardiomyocytes to a dedifferentiated state', PLoS ONE, vol. 16, no. 5, e0251054. https://doi.org/10.1371/journal.pone.0251054

APA

Kisby, T., De Lázaro, I., Stylianou, M., Cossu, G., Kostarelos, K., & Asakura, A. (Ed.) (2021). Transient reprogramming of postnatal cardiomyocytes to a dedifferentiated state. PLoS ONE, 16(5), [e0251054]. https://doi.org/10.1371/journal.pone.0251054

Vancouver

Author

Kisby, Thomas ; De Lázaro, Irene ; Stylianou, Maria ; Cossu, Giulio ; Kostarelos, Kostas ; Asakura, Atsushi (Editor). / Transient reprogramming of postnatal cardiomyocytes to a dedifferentiated state. In: PLoS ONE. 2021 ; Vol. 16, No. 5.

Bibtex

@article{29deccd4947f4008975f16e5659af101,
title = "Transient reprogramming of postnatal cardiomyocytes to a dedifferentiated state",
abstract = "In contrast to mammals, lower vertebrates are capable of extraordinary myocardial regeneration thanks to the ability of their cardiomyocytes to undergo transient dedifferentiation and proliferation. Somatic cells can be temporarily reprogrammed to a proliferative, dedifferentiated state through forced expression of Oct3/4, Sox2, Klf4 and c-Myc (OSKM). Here, we aimed to induce transient reprogramming of mammalian cardiomyocytes in vitro utilising an OSKM-encoding non-integrating vector. Reprogramming factor expression in postnatal rat and mouse cardiomyocytes triggered rapid but limited cell dedifferentiation. Concomitantly, a significant increase in cell viability, cell cycle related gene expression and Ki67 positive cells was observed consistent with an enhanced cell cycle activation. The transient nature of this partial reprogramming was confirmed as cardiomyocyte-specific cell morphology, gene expression and contractile activity were spontaneously recovered by day 15 after viral transduction. This study provides the first evidence that adenoviral OSKM delivery can induce partial reprogramming of postnatal cardiomyocytes. Therefore, adenoviral mediated transient reprogramming could be a novel and feasible strategy to recapitulate the regenerative mechanisms of lower vertebrates.",
author = "Thomas Kisby and {De L{\'a}zaro}, Irene and Maria Stylianou and Giulio Cossu and Kostas Kostarelos and Atsushi Asakura",
year = "2021",
month = may,
day = "5",
doi = "10.1371/journal.pone.0251054",
language = "English",
volume = "16",
journal = "PL o S One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "5",

}

RIS

TY - JOUR

T1 - Transient reprogramming of postnatal cardiomyocytes to a dedifferentiated state

AU - Kisby, Thomas

AU - De Lázaro, Irene

AU - Stylianou, Maria

AU - Cossu, Giulio

AU - Kostarelos, Kostas

A2 - Asakura, Atsushi

PY - 2021/5/5

Y1 - 2021/5/5

N2 - In contrast to mammals, lower vertebrates are capable of extraordinary myocardial regeneration thanks to the ability of their cardiomyocytes to undergo transient dedifferentiation and proliferation. Somatic cells can be temporarily reprogrammed to a proliferative, dedifferentiated state through forced expression of Oct3/4, Sox2, Klf4 and c-Myc (OSKM). Here, we aimed to induce transient reprogramming of mammalian cardiomyocytes in vitro utilising an OSKM-encoding non-integrating vector. Reprogramming factor expression in postnatal rat and mouse cardiomyocytes triggered rapid but limited cell dedifferentiation. Concomitantly, a significant increase in cell viability, cell cycle related gene expression and Ki67 positive cells was observed consistent with an enhanced cell cycle activation. The transient nature of this partial reprogramming was confirmed as cardiomyocyte-specific cell morphology, gene expression and contractile activity were spontaneously recovered by day 15 after viral transduction. This study provides the first evidence that adenoviral OSKM delivery can induce partial reprogramming of postnatal cardiomyocytes. Therefore, adenoviral mediated transient reprogramming could be a novel and feasible strategy to recapitulate the regenerative mechanisms of lower vertebrates.

AB - In contrast to mammals, lower vertebrates are capable of extraordinary myocardial regeneration thanks to the ability of their cardiomyocytes to undergo transient dedifferentiation and proliferation. Somatic cells can be temporarily reprogrammed to a proliferative, dedifferentiated state through forced expression of Oct3/4, Sox2, Klf4 and c-Myc (OSKM). Here, we aimed to induce transient reprogramming of mammalian cardiomyocytes in vitro utilising an OSKM-encoding non-integrating vector. Reprogramming factor expression in postnatal rat and mouse cardiomyocytes triggered rapid but limited cell dedifferentiation. Concomitantly, a significant increase in cell viability, cell cycle related gene expression and Ki67 positive cells was observed consistent with an enhanced cell cycle activation. The transient nature of this partial reprogramming was confirmed as cardiomyocyte-specific cell morphology, gene expression and contractile activity were spontaneously recovered by day 15 after viral transduction. This study provides the first evidence that adenoviral OSKM delivery can induce partial reprogramming of postnatal cardiomyocytes. Therefore, adenoviral mediated transient reprogramming could be a novel and feasible strategy to recapitulate the regenerative mechanisms of lower vertebrates.

U2 - 10.1371/journal.pone.0251054

DO - 10.1371/journal.pone.0251054

M3 - Article

VL - 16

JO - PL o S One

JF - PL o S One

SN - 1932-6203

IS - 5

M1 - e0251054

ER -