Inhibition of notch1-dependent cardiomyogenesis leads to a dilated myopathy in the neonatal heart.

ABSTRACT:

Rationale

Physiological hypertrophy in the developing heart has been considered the product of an increase in volume of preexisting fetal cardiomyocytes in the absence of myocyte formation.

Objective

In this study, we tested whether the mouse heart at birth has a pool of cardiac stem cells (CSCs) that differentiate into myocytes contributing to the postnatal expansion of the parenchymal cell compartment.

Methods and results

We have found that the newborn heart contains a population of c-kit-positive CSCs that are lineage negative, self-renewing, and multipotent. CSCs express the Notch1 receptor and show the nuclear localization of its active fragment, N1ICD. In 60% of cases, N1ICD was coupled with the presence of Nkx2.5, indicating that the commitment of CSCs to the m

SUBMITTER: Urbanek K 

PROVIDER: S-EPMC2919068 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature