Relationship between fibronectin expression during gastrulation and heart formation in the rat embryo

Abstract

By utilizing myosin immunostaining, we were able to identify early rat myocardium as a thin epithelial sheet and realized that its cohesive movement toward the midline leads to the straight heart tube formation. Localization study of fibronectin mRNA and protein was, therefore, carried out to investigate its tissue origin and possible roles in facilitating mesoderm migration and heart formation. Fibronectin mRNAs were first detected throughout the mesoderm during the early primitive streak stage, suggesting that the mesoderm is the source of fibronectin. By pre-head fold (pre-somite) and head fold (early somite) stages, the mesoderm became largely down-regulated for fibronectin mRNAs, while it was also at these stages when myosin-positive myocardium formed itself into the epithelium and was subsequently folding toward the midline. Thus, there appears to be little fibronectin synthesis during and directly relevant to early heart tube formation. Later, during the early straight heart tube stage (5 somite and older), endocardium became highly positive for fibronectin mRNAs, suggesting that the endocardium is the major source of fibronectin for the cardiac jelly. Based on the results, we present a map for the early mammalian heart in which the heart is a single crescentic band lying in front of the prechordal plate. We also suggest a process for heart tube formation based on the cohesive movement of the myocardial epithelium. During heart tube formation, fibronectin protein had been deposited previously by the mesoderm and was found uniformly in the ECM and not newly produced by any adjacent tissue. The data contradict the endodermal guidance of heart migration by fibronectin gradient and suggest, instead, a permissive role for the fibronectin substrate. o 1996 Wiley-Liss, Inc.

Hyperglycemia‐induced TGFβ and fibronectin expression in embryonic mouse heart

“…FN functions in cell-cell and cell-ECM interactions, embryonic differentiation, wound healing, and neoplastic transformation (McDonagh, 1981;Dufour et al, 1988). In the rat embryo, FN mRNA expression is elevated in the endocardium of the early heart tube, and FN protein later becomes uniformly distributed in the ECM (cardiac jelly) between the myocardium and endocardium of the heart tube (Suzuki et al, 1995). FN is important in the migration of precardiac cells and the development of cardiac cushion cells (Linask and Lash, 1986;Icardo et al, 1992).…”

Requirement of the transcription factor GATA4 for heart tube formation and ventral morphogenesis.

“…DeHaan (1963) concluded that the active process resulting in lateral to ventral folding at the level of the AIP likely occurs as a result of the mobility of clusters of precardiac cells. However, more recent evidence suggests that the underlying endoderm may also participate in this process (Suzuki et al 1995). Thus, it is likely that the process of lateral to ventral folding occurs as a result of an interplay between the overlying splanchnic mesoderm and the underlying endoderm, possibly because of differential growth between these two layers and the embryo proper.…”

Increased Fibronectin Deposition in Embryonic Hearts of Retinol-Binding Protein–Null Mice

“…During heart development, Fn substrates are required to support the migration of precardiac mesoderm during gastrulation 31,32 and mesenchymal cells during cushion formation. 33 Curiously, in situ hybridization ( Figure 5) has suggested that cardiac jelly Fn is strongly expressed by endocardial cells with virtually no contribution from the myocardium; because Fn is expressed by early myocardial cells in chick embryos, 20 hybridization at earlier stages in mouse development will clarify this issue.…”

“…28 It is of interest that Fn expression in adult myocytes and cardiac fibroblasts is strongly regulated by cytokines. 29,30 Hence, we are investigating the Fn phenotype in RBP-null embryos using a microarray approach to identify (1) matrix components that may be misregulated and (2) possible roles for extracellular proteases and protease inhibitors.During heart development, Fn substrates are required to support the migration of precardiac mesoderm during gastrulation 31,32 and mesenchymal cells during cushion formation. 33 Curiously, in situ hybridization ( Figure 5) has suggested that cardiac jelly Fn is strongly expressed by endocardial cells with virtually no contribution from the myocardium; because Fn is expressed by early myocardial cells in chick embryos, 20 hybridization at earlier stages in mouse development will clarify this issue.…”

“…generated a 665 nt antisense riboprobe labeled with [α- 32 P]-UTP. Riboprobe was purified using the RNeasy kit and 5 x10 6 cpm per ml were diluted in NorthernMax hybridization solution (Ambion).…”