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Demonstrates normal epicardial epithelial-to-mesenchymal transition despite Snail1 deletion in mice, indicating Snail1 is dispensable for embryonic heart development.
The epicardium is the outer epithelial covering the heart. This tissue undergoes an epithelial-to-mesenchymal transition (EMT) to generate mesenchymal epicardial-derived cells (EPDCs) that populate the extracellular matrix of the subepicardium and contribute to the development of the coronary vessels and cardiac interstitial cells. Although epicardial EMT plays a crucial role in heart development, the molecular regulation of this process is incompletely understood. Here we examined the possible role of the EMT regulator Snail1 in this process. Snail1 is expressed in the epicardium and EPDCs during mouse cardiac development. To determine the function of Snail1 in epicardial EMT, we deleted Snail1 in the epicardium using Wt1- and Tbx18-Cre drivers. Unexpectedly, epicardial-specific Snail1 mutants are viable and fertile and do not display any obvious morphological or functional cardiac abnormalities. Molecular analysis of these mice reveals that epicardial EMT occurs normally, and epicardial derivatives are established in these mutants. We conclude that Snail1 is not required for the initiation and progression of embryonic epicardial EMT.
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Casanova et al. (2012) studied this question.
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