Stem Cells Dev 2004 Dec 01;136:614-24. doi: 10.1089/scd.2004.13.614.

An in vitro analysis of myocardial potential indicates that phenotypic plasticity is an innate property of early embryonic tissue.

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Explants from gastrula-stage avian embryos have provided an important culture model for examining the formation of the vertebrate heart. Explants harvested from anterior regions containing the precardiac mesoderm faithfully recapitulate cardiogenesis and generate contractile tissue in culture. Posterior regions of the early embryo do not supply cellular material to the developing heart in situ, and thus have been commonly employed as negative control tissues for studying cardiogenic induction. To begin to understand the cellular mechanisms that account for the distinct cell fates of precardiac and posterior tissue within the embryo, we undertook a comprehensive investigation on the myocardial potential of presumptive noncardiac tissue. Myocardial differentiation was assayed by expression of the myocardium-associated transcription factor gene Nkx2.5 and positive immunostaining for sarcomeric myosin, muscle alpha-actinin, and smooth muscle alpha-actin. Our results demonstrate that regions of the early embryo that do not provide a cellular contribution to the myocardium in situ are capable of generating myocardial tissue when removed from their normal embryonic environment and placed in culture under nontreated conditions. Although treatment with the presumptive cardiac inducer Dickkopf-1 increased the frequency that cardiac tissue appeared within cultures of posterior tissue, no difference was observed in either the size or morphology of the myocardium-positive areas among treated and nontreated explants. These findings suggest that progenitor cells within the early embryo possess an innate phenotypic plasticity and that presumptive cardiac inducing signals do not induce cardiac differentiation but instead augment a pre-existing cardiac potential of embryonic tissue.

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Species referenced: Xenopus
Genes referenced: acta2 actl6a actn1