Role of extracardiac factors in heart development

Abstract

Many factors extrinsic to the developing heart play important roles in determining its final form. The neural crest has been shown to provide ectomesenchyme to the pharyngeal apparatus and outflow tract, as well as the postganglionic innervation of the heart. Ablation of the neural crest providing ectomesenchyme to the outflow tract results in various cardiac malformations. These malformations have in common either outflow and/or inflow tract malalignment. Although the reason for this malalignment is not understood, it is thought that hemodynamic parameters during early cardiac morphogenesis may be disrupted causing cardiac dysmorphogenesis. The most likely area for this alteration to occur is in the pharyngeal apparatus which houses the aortic arch arteries. Various possibilities are discussed. The innervation of the heart by neural crest-derived autonomic neurons and nodose placode-derived sensory neurons is outlined, and the interactions between the two progenitive sites is discussed.

Expression of epidermal growth factor family gene members in early mouse development

“…Septation of the heart outflow tract involves neural crest-derived ectomesenchyme cells. In the chick, ablation of the cardiac neural crest before it migrates results in persistent truncus arteriosus, a condition in which only a single arterial vessel arises from the heart (Kirby, 1988). Since Cripto is expressed so specifically in the outflow tract myocardium, it may be involved in spatial signaling for these migrating neural crest cells.…”

Expression of intermediate filament desmin and vimentin in the human fetal heart

“…In brief, the heart begins to beat concomitantly with the formation of the heart tube and the initiation of looping, and then cardiac function is established by hemodynamic effects (e.g., vascular resistance), innervation, seeding of the outflow tract with extracardially derived ectomesenchyme, circulating factors such as polypeptides and hormones, and neural crest association (Kirby, 1988); therefore, this organ is exposed to constant stimuli including tension by contraction-relaxation, hemodynamic forces, and neurohumoral factors of extrinsic and/or intrinsic origins. Occasionally, these conditions may be hazardous and could impair either structure or function (Steenbergen et al, 1987;Iwai et al, 1990).…”

Prenatal Craniofacial Development: New Insights On Normal and Abnormal Mechanisms

“…If, prior to their migration, second-arch crest cells are replaced with first-arch crest cells, they migrate into the second arch but still form first-arch skeletal elements in response to the second-arch environment (Noden, 1983b). Also, if crest cells that normally form a major portion of the septal mesenchyme of the cono-truncus are replaced by other cranial neural crest cells, the substituted cells are unable to form this mesenchyme (Kirby, 1988).…”

“…A common feature of these syndromes, including the RAS (and, apparently, many thalidomide malformations), is a high incidence of cardiovascular malformations of the cono-truncal variety. The significance of this association was greatly clarified by the findings of Kirby et al (1983) that cranial neural crest cells form much of the mesenchyme of the cono-truncal septum and that extirpation of these cells prior to their migration leads to cardiovascular malformations of the conotruncal type (see also Kirby, 1988, for review of additional studies). This suggests that defects in crest cell formation and/or migration may play a major role in many of these malformation complexes.…”