Precardiac cell migration: Fibronectin localization at mesoderm-endoderm interface during directional movement

Four types of microsurgical experiments were conducted to analyze heart and blood vessel development during gastrula stages of avian embryos, stages during which prospective cardiogenic and vasculogenic cells reside within the primitive streak. Experiments addressed whether cells not normally destined to form heart could form heart when given the opportunity to do so and vice versa; cells destined to form rostral levels of the heart (or, alternatively, head blood vessels) could form caudal levels of the heart (or, alternatively, trunk blood vessels) and vice versa; the early endoderm imparts rostrocaudal organization to the heart and associated blood vessels; and ingression of cells from the primitive streak and their subsequent migration into the mesodermal mantle is a cell-autonomous event for migrating cells. Our results demonstrate the lability of prospective cardiogenic and vasculogenic cells of the primitive streak, both in terms of the type of mesodermal structures they are capable of forming (or of being formed from) and in terms of the rostrocaudal patterning of the cardiovascular system. In addition, our results show that cell ingression and migration is directed by environmental cues and is not a cell-autonomous process for migrating cells. Finally, our results suggest that patterning of the. cardiovascular system occurs after cells enter the mesodermal mantle, presumably through cell-cell inductive interactions. However, the early endoderm is not the primary source of the patterning influence. What is the source remains to be established. %, 1993 Wiley-Liss, Inc.

Section: Discussionmentioning

confidence: 60%

Regulative ability of the prospective cardiogenic and vasculogenic areas of the primitive streak during avian gastrulation

Inagaki

García‐Martínez

Schoenwolf

1993

“…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). Inhibiting the activity of matrix metalloproteinases, enzymes that digest ECM proteins, blocks effective migration of precardiac neural crest cells (Cai and Brauer, 2002), supporting a role for increased ECM proteins in the pathogenesis of cardiac defects.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia‐induced TGFβ and fibronectin expression in embryonic mouse heart

Smoak

2004

Cardiovascular defects are common in diabetic offspring, but their etiology and pathogenesis are poorly understood. Extracellular matrix accumulates in adult tissues in response to hyperglycemia, and transforming growth factor-beta1 (TGF␤1) likely mediates this effect. The objective of this study was to characterize TGF␤ expression in the organogenesisstage mouse heart and to evaluate TGF␤ and fibronectin expression in embryonic mouse heart exposed to hyperglycemia. Prominent TGF␤1, and minimal TGF␤2 or TGF␤3, protein expression was demonstrated in embryonic day (E) 9.5-E13.5 hearts. Hyperglycemia for 24 hr produced significantly increased fibronectin, slightly increased TGF␤1, and unchanged TGF␤2 or TGF␤3, by immunohistochemistry. Increased TGF␤1 was demonstrated by enzyme-linked immunosorbent assay in embryonic fluid and isolated hearts after hyperglycemia for 24 hr, but not 48 hr. Hyperglycemia increased fibronectin protein and mRNA expression in embryonic hearts after 24 hr, and pericardial injection of TGF␤1 also increased fibronectin mRNA in the embryonic heart. It is proposed that TGF␤1 and fibronectin may play a role in diabetes-induced cardiac dysmorphogenesis.

“…Linask and Lash (1986) reported that fibronectin was found in increasing amounts toward the anterior end of the embryo and suggested that such gradient of fibronectin distribution is responsible for the anterior migration of the cardiogenic mesoderm. They also partially blocked the normal process of heart tube formation by adding an anti-fibronectin antibody to the embryo (Linask and Lash, 1988a).…”

Section: Introductionmentioning

confidence: 99%

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

Suzuki

Solursh

Baldwin

1995

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.