Abstract：
:Cardiogenesis depends on a tightly regulated balance between proliferation and differentiation of cardiac progenitor cells (CPCs) and their cardiomyocyte descendants. While exposure of early mouse embryos to Ca(2+) channel antagonists has been associated with abnormal cardiac morphogenesis, less is known about the consequences of Ca(2+) channel blockade on proliferation and differentiation of CPCs at the cellular level. Here we showed that at embryonic day (E) 11.5, the murine ventricles express several L-type and T-type Ca(2+) channel isoforms, and that the dihydropyridine Ca(2+) channel antagonist, nifedipine, blunts isoproterenol induced increases in intracellular Ca(2+). Nifedipine mediated Ca(2+) channel blockade was associated with a reduction in cell cycle activity of E11.5 CPCs and impaired assembly of the cardiomyocyte contractile apparatus. Furthermore, in cell transplantation experiments, systemic administration of nifedipine to adult mice receiving transplanted E11.5 ventricular cells (containing CPCs and cardiomyocytes) was associated with smaller graft sizes compared to vehicle treated control animals. These data suggest that intracellular Ca(2+) is a critical regulator of the balance between CPC proliferation and differentiation and demonstrate that interactions between pharmacological drugs and transplanted cells could have a significant impact on the effectiveness of cell based therapies for myocardial repair.
journal_name
Cell Calciumjournal_title
Cell calciumauthors
Hotchkiss A,Feridooni T,Zhang F,Pasumarthi KBdoi
10.1016/j.ceca.2014.02.018subject
Has Abstractpub_date
2014-05-01 00:00:00pages
238-51issue
5eissn
0143-4160issn
1532-1991pii
S0143-4160(14)00040-2journal_volume
55pub_type
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