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

First Author  Liu X Year  2015
Journal  Nat Commun Volume  6
Pages  8825 PubMed ID  26593099
Mgi Jnum  J:228012 Mgi Id  MGI:5704258
Doi  10.1038/ncomms9825 Citation  Liu X, et al. (2015) Rescue of neonatal cardiac dysfunction in mice by administration of cardiac progenitor cells in utero. Nat Commun 6:8825
abstractText  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.
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