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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.

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