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Rescue of neonatal cardiac dysfunction in mice by administration of cardiac progenitor cells in utero

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  • Xiaoli Liu

    (Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
    Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Sean R. R. Hall

    (Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Zhihong Wang

    (Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • He Huang

    (Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Sailaja Ghanta

    (Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Moises Di Sante

    (Cardiovascular Medicine, Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
    Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Annarosa Leri

    (Cardiovascular Medicine, Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
    Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Piero Anversa

    (Cardiovascular Medicine, Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
    Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

  • Mark A. Perrella

    (Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
    Brigham and Women’s Hospital and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA)

Abstract

Striated preferentially expressed gene (Speg) is a member of the myosin light chain kinase family. We previously showed that disruption of the Speg gene locus in mice leads to a dilated cardiomyopathy with immature-appearing cardiomyocytes. Here we show that cardiomyopathy of Speg−/− mice arises as a consequence of defects in cardiac progenitor cell (CPC) function, and that neonatal cardiac dysfunction can be rescued by in utero injections of wild-type CPCs into Speg−/− foetal hearts. CPCs harvested from Speg−/− mice display defects in clone formation, growth and differentiation into cardiomyocytes in vitro, which are associated with cardiac dysfunction in vivo. In utero administration of wild-type CPCs into the hearts of Speg−/− mice results in CPC engraftment, differentiation and myocardial maturation, which rescues Speg−/− mice from neonatal heart failure and increases the number of live births by fivefold. We propose that in utero administration of CPCs may have future implications for treatment of neonatal heart diseases.

Suggested Citation

  • Xiaoli Liu & Sean R. R. Hall & Zhihong Wang & He Huang & Sailaja Ghanta & Moises Di Sante & Annarosa Leri & Piero Anversa & Mark A. Perrella, 2015. "Rescue of neonatal cardiac dysfunction in mice by administration of cardiac progenitor cells in utero," Nature Communications, Nature, vol. 6(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9825
    DOI: 10.1038/ncomms9825
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