Abstract

In the developing vertebrate heart, cells that contribute to vascular smooth muscle, cardiac fibroblasts, and coronary endothelial cells are derived from the proepicardium and associated cells originally located at the venous pole of the primitive heart tube. Recently, there has been much interest in the regulatory mechanisms that control epicardium-derived cell (EPDC) lineage development and mobilization with adult cardiac injury. However, less is known of the embryonic origins and inductive mechanisms that control the initial induction of the proepicardium. The study by Schlueter and Brand1 in the current issue of Circulation Research reports fate mapping of proepicardial progenitors to the somatic mesoderm and demonstrates a critical role for the basic helix-loop-helix transcription factor Twist1 in the earliest stages of proepicardial development. Article, see p 1128 The heart is the first organ to function in the developing vertebrate embryo, and beating of the primitive heart tube is apparent by embryonic day (E)8 in mouse and by 40 hours of development in chicken embryos.2 As the primitive heart tube loops, lateral plate mesoderm cells on the right side of the embryo at the cardiac venous pole begin to form the proepicardium.3 Schlueter and Brand1 demonstrate through fate mapping studies in avian embryos that at least some cells of the proepicardium are derived from the somatic layer of lateral plate mesoderm. The somatic compartment (somatopleure) of the lateral plate mesoderm is adjacent to the ectoderm and forms the body wall.4 The new data provide initial evidence that cells of the proepicardium also are derived from somatic mesodermal layer. The proepicardium shares many characteristics with other mesothelia of the major coelomic organs that contribute progenitors of fibroblasts and smooth muscle to the lung, gut, kidney, etc.4 The embryonic origins of coelomic mesothelia are not …

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