Prenatal development of coronary arteries in the rat: morphologic patterns

Ratajska, Anna; Fiejka, E

doi:10.1007/s004290050301

Cited by 33 publications

(46 citation statements)

References 33 publications

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“…The NRBCs residing in blood islands express Ter/119 antigen, whereas endothelial cells exhibited PECAM1 antigen. In addition to the previous TEM studies (Rongish et al, 1994;Ratajska and Fiejka, 1999), which claimed that red blood cells were accompanied by angioblasts/endothelial cells, we demonstrated that some of the NRBCs were located in areas where angioblasts were absent. These solitary (free) NRBCs were mostly positioned in the subendocardium.…”

Section: Myocardium and Subepicardiumsupporting

confidence: 76%

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Vasculogenesis of the embryonic heart: Origin of blood island‐like structures

et al. 2006

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The earliest vascular structures (blood island-like) in the embryonic heart are clusters of angioblasts and nucleated red blood cells (NRBCs), which differentiate into endothelial cells and erythrocytes, respectively. Our purpose was to define the area and chronology of NRBC appearance in the mouse embryonic heart at the stages before a patency between coronary vessels and peripheral circulation is established (10.5-13.5 dpc). Before and at the onset of vascularization, NBCs were not present within the proepicardium; however, Ter/119 ϩ differentiating erythroblasts and single scattered CD45 ϩ were found in the heart beginning from 10.5 dpc. The Ter/119 ϩ cells were in close apposition to angioblasts (PECAM1 ϩ ) and were recognized as components of blood island-like structures or vascular vesicles in transmission electron microscope and were located mostly in the subepicardium. Some of the NRBCs were not accompanied by angioblasts and located close to the endocardial endothelium or at the border of the endocardial endothelium or in the subepicardium. These erythroblasts were beginning to assemble with angioblasts. CD34 ϩ NBCs as well as progenitor cells of erythroid lineage were not detected in the heart at these stages of development. The state of differentiation of NRBCs of blood islands was similar/the same as the morphology of circulating blood cells at the respective stages of embryo development. The presence of mature NRBCs in the subendocardial area and lack of progenitor cells of erythroid lineage within the heart indicate that erythroid commitment occurs outside the heart. We suggest that NRBCs enter the heart from the blood stream at 10.5-12 dpc independently from angioblasts.

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Section: Myocardium and Subepicardiumsupporting

confidence: 76%

“…Blood island-like structures are located within the myocardial wall and the subepicardium of 10 and 11 dpc mice (Virá gh and Challice, 1981). They are encountered within 13 dpc rat hearts (Rongish et al, 1994;Ratajska and Fiejka, 1999). They are also found in the embryonic heart in later stages of development (until full term).…”

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confidence: 99%

Vasculogenesis of the embryonic heart: Origin of blood island‐like structures

et al. 2006

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“…In the prenatal and postnatal hearts of rat and mice, the coronary arteries have a completely intramyocardial course, whereas the coronary veins have a subepicardial course (53,54). Both types of coronary vessels have typical branching patterns and are connected either to the aorta (coronary arteries) or the sinus venosus (coronary veins).…”

Section: Generation Of Epicardium-restrictedmentioning

confidence: 99%

Epicardium-derived progenitor cells require β-catenin for coronary artery formation

Zamora

Männer²,

Ruiz‐Lozano³

2007

Proc. Natl. Acad. Sci. U.S.A.

156

136

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We have previously identified several members of the Wnt/␤-catenin pathway that are differentially expressed in a mouse model with deficient coronary vessel formation. Systemic ablation of ␤-catenin expression affects mouse development at gastrulation with failure of both mesoderm development and axis formation. To circumvent this early embryonic lethality and study the specific role of ␤-catenin in coronary arteriogenesis, we have generated conditional ␤-catenin-deletion mutant animals in the proepicardium by interbreeding with a Cre-expressing mouse that targets coronary progenitor cells in the proepicardium and its derivatives. Ablation of ␤-catenin in the proepicardium results in lethality between embryonic day 15 and birth. Mutant mice display impaired coronary artery formation, whereas the venous system and microvasculature are normal. Analysis of proepicardial ␤-catenin mutant cells in the context of an epicardial tracer mouse reveals that the formation of the proepicardium, the migration of proepicardial cells to the heart, and the formation of the primitive epicardium are unaffected. However, subsequent processes of epicardial development are dramatically impaired in epicardial-␤-catenin mutant mice, including failed expansion of the subepicardial space, blunted invasion of the myocardium, and impaired differentiation of epicardium-derived mesenchymal cells into coronary smooth muscle cells. Our data demonstrate a functional role of the epicardial ␤-catenin pathway in coronary arteriogenesis. The embryonic epicardium originates from a primarily extracardiac primordium, the proepicardum, which is located at the septum transversum near the venous pole of the heart (2, 3). In mouse embryos, proepicardial cells reach the heart predominantly in the form of free-floating vesicles that traverse the pericardial cavity, adhere to the initially naked myocardial surface, and subsequently form the epicardial covering of the heart (reviewed in ref. 1). The recruitment of coronary vessel progenitor cells from the proepicardium and embryonic epicardium involves several steps of epithelial-mesenchymal transition (EMT). As a result of proepicardial EMT, the extracellular matrix of free-floating proepicardial vesicles becomes populated with mesenchymal cells (4-8). Subsequently, the primitive epicardium gives rise to the subepicardial mesenchyme, also by means of EMT.Recent data suggest that the primitive epicardium and epicardium-derived cells (EPDCs) modulate the maturation of other cardiac components, including the embryonic myocardium and the cardiac conduction system (9-14). We have previously shown that the embryonic epicardium is a key signaling tissue responsible for the transmission of the morphogenic signal derived from retinoic acid and identified several components of the Wnt/␤-catenin signaling pathway that are down-regulated upon retinoid signaling deficiency, in particular, ␤-catenin and its activator Wnt9b (15).However, it remains to be shown whether Wnt/␤-catenin signaling plays a specific role in the de...

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“…Subsequently, the myocardial wall thickens, and trabeculae gradually become flatter and wider (Ošt'á dal et al, 1975). On ED16 -17, coronary arteries form patent connections with the aorta (Bogers et al, 1988;Ratajska and Fiejka, 1999), and probably at about the same time (based on the studies in quail heart by Vrancken Peeters et al (1997a) the venous system forms a connection with the right atrium.…”

mentioning

confidence: 96%

Embryonic development of coronary vasculature in rats: Corrosion casting studies

2003

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The aim of this study was to analyze the development of coronary vessels at different stages of embryonic life in rats using corrosion casts and scanning electron microscopy (SEM). We studied morphologic details of vessel maturation, expansion, and pattern formation from the stage of development when the coronary system forms patent connections with the aorta and the right atrium (embryonic day 16 (ED16)) to full-term fetus (ED21). The internal surface morphologies of the arterial and venous vessel walls were different and were dependent on the distance from the orifice and the capillary system. They also depended on the maturation state of a given vessel. In various branches of the coronary system we demonstrated round, fusiform or polygonal, endothelial cell imprints. The capillary network was dense, however, at the early stages of development, it formed a thin layer over the myocardium. By ED21 capillaries assumed an orientation parallel to the long axes of the cardiac myocytes. During all stages of development, different forms of angiogenesis by intussusceptive growth were observed. Splitting of the vessel wall occurred in two or three points along the vessel, forming two-or three-link chains. Certain areas of vessels resembled doughnuts, from which several sister vessels originated. The coronary arteries were situated deep within the myocardial wall. The major coronary veins were mostly located on the surface of the capillary plexuses of the myocardial wall. In conclusion, this method of vessel casting enables the detection of angiogenesis by intussusceptive growth, and the visualization of a capillary's position to the myocardial wall, thickness of the capillary plexuses, and the internal surface morphology of major vessels. Anat Rec Part A 270A: 109 -116, 2003.

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Prenatal development of coronary arteries in the rat: morphologic patterns

Cited by 33 publications

References 33 publications

Vasculogenesis of the embryonic heart: Origin of blood island‐like structures

Vasculogenesis of the embryonic heart: Origin of blood island‐like structures

Epicardium-derived progenitor cells require β-catenin for coronary artery formation

Embryonic development of coronary vasculature in rats: Corrosion casting studies

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