Distribution of the neural crest cells in the heart of birds: a three dimensional analysis

Sumida, Hiroshi; Akimoto, Naotaka; Nakamura, Harukazu

doi:10.1007/bf00321897

Cited by 67 publications

(60 citation statements)

References 9 publications

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“…The origin of the cells within the AP septum is different from that of cushion mesenchymal cells. Migrating cells withhin the AP septum derive from the neural crest (KIRBY et al, 1983;SUMIDA et al, 1989b), and are fibronectin receptor-rich (SUMIDA et al, 1989a). Thus, it is suggested that cells which have the fibronectin receptor migrate into the fibronectin-rich pathways, and cells which have the vitronectin receptor migrate into vitronectin-rich pathways.…”

Section: Discussionmentioning

confidence: 99%

Distribution of vitronectin in the embryonic chick heart during endocardial cell migration.

Sumida

Nakamura

Satow

1990

Arch. Histol. Cytol.

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Summary. In the early phase of heart development, the endocardial cells migrate into the truncal swellings and atrioventricular (AV) cushions, and become mesenchymal cells. Vitronectin is a glycoprotein which is thought to mediate cell migration. The present study demonstrates by immunohistochemistry the distribution of vitronectin in order to elucidate its contribution to endocardial cell migration in the developing chick heart.At HAMBURGER and MAMILTON's stage 23, the network of fibrillar material filled the extracellular space of both truncal swellings and AV cushions. The fibrillar network has been thought to be a matrix for endocardial cell migration. The network was stained with the anti-vitronectin antibody. At stage 29, the swellings and cushions were packed with mesenchymal cells, though immunoreactivity to the antibody was still observed in the extracellular matrix. The myocardium facing the AV cushions reacted to the antibody, but the myocardium surrounding the truncus arteriosus did not. The intensity of the immunohistochemical staining of the myocardium facing the AV cushions increased and reached a peak at stages 24 to 26, and then became weak by stage 29. The endocardial sheet, aortico-pulmonary septum and developing tunica media of the great arteries were not stained by the antibody at any stage.These results strongly suggest that vitronectin is involved in the migration of endocardial cells, and that the myocardium facing the AV cushions produces vitronectin.

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Section: Discussionmentioning

confidence: 99%

Distribution of vitronectin in the embryonic chick heart during endocardial cell migration.

Sumida

Nakamura

Satow

1990

Arch. Histol. Cytol.

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“…These heart cartilages have, however, NC, but not the mesoderm origin at least in birds and mammals (Sumida et al, 1989). Although axolotl belongs to amphibians, the proximity of the anlagen of the heart and the prospective basibranchial 2, both of which show, or cells of different embryonic origin, may indicate a possibility of a cartilaginous differentiation of both NC derived ectomesenchyme and LPM.…”

Section: Chial 2 Cartilagementioning

confidence: 98%

Dual embryonic origin of the hyobranchial apparatus in the Mexican axolotl (Ambystoma mexicanum)

Davidian

Malashichev

2013

Int. J. Dev. Biol.

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Traditionally, the cartilaginous viscerocranium of vertebrates is considered as neural crest (NC)-derived. Morphological work carried out on amphibian embryos in the first half of the XX century suggested potentially mesodermal origin for some hyobranchial elements. Since then, the embryonic sources of the hyobranchial apparatus in amphibians has not been investigated due to lack of an appropriate long-term labelling system. We performed homotopic transplantations of neural folds along with the majority of cells of the presumptive NC, and/or fragments of the head lateral plate mesoderm (LPM) from transgenic GFP+ into white embryos. In these experiments, the NC-derived GFP+ cells contributed to all hyobranchial elements, except for basibranchial 2, whereas the grafting of GFP+ head mesoderm led to a reverse labelling result. The grafting of only the most ventral part of the head LPM resulted in marking of the basibranchial 2 and the heart myocardium, implying their origin from a common mesodermal region. This is the first evidence of contribution of LPM of the head to cranial elements in any vertebrate. If compared to fish, birds, and mammals, in which all branchial skeletal elements are NC-derived, the axolotl (probably this is true for all amphibians) demonstrates an evolutionary deviation, in which the head LPM replaces NC cells in a hyobranchial element. This implies that cells of different embryonic origin may have the same developmental program, leading to the formation of identical (homologous) elements of the skeleton.

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“…They include persistent truncus arteriosus and transposition of the great vessels. In the outflow tract, the cardiac neural crest cells form two opposing spiraling ridges that grow together and eventually merge, dissecting the single outflow tract tube into two vessels, the aorta and the pulmonary artery (Sumida et al, 1989). A distinct population of either neural crest cells or ventrally derived rhombencephalic cells enters the heart at the venous pole.…”

Section: The Cardiac Neural Crestmentioning

confidence: 99%

Cardiac neural crest stem cells

Sieber‐Blum

2003

Anat. Rec.

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Whereas the heart itself is of mesodermal origin, components of the cardiac outflow tract are formed by the neural crest, an ectodermal derivative that gives rise to the peripheral nervous system, endocrine cells, melanocytes of the skin and internal organs, and connective tissue, bone, and cartilage of the face and ventral neck, among other tissues. Cardiac neural crest cells participate in the septation of the cardiac outflow tract into aorta and pulmonary artery. The migratory cardiac neural crest consists of stem cells, fate-restricted cells, and cells that are committed to the smooth muscle cell lineage. During their migration within the posterior branchial arches, the developmental potentials of pluripotent neural crest cells become restricted. Conversely, neural crest stem cells persist at many locations, including in the cardiac outflow tract. Many aspects of neural crest cell differentiation are driven by growth factor action. Neurotrophin-3 (NT-3) and its preferred receptor, TrkC, play important roles not only in nervous system development and function, but also in cardiac development as deletion of these genes causes outflow tract malformations. In vitro clonal analysis has shown a premature commitment of cardiac neural crest stem cells in TrkC null mice and a perturbed morphology of the endothelial tube. Norepinephrine transporter (NET) function promotes the differentiation of neural crest stem cells into noradrenergic neurons. Surprisingly, many diverse nonneuronal embryonic tissues, in particular in the cardiovascular system, express NET also. It will be of interest to determine whether norepinephrine transport plays a role also in cardiovascular development. Anat Rec Part A 276A: 34 -42, 2004.

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Distribution of the neural crest cells in the heart of birds: a three dimensional analysis

Cited by 67 publications

References 9 publications

Distribution of vitronectin in the embryonic chick heart during endocardial cell migration.

Distribution of vitronectin in the embryonic chick heart during endocardial cell migration.

Dual embryonic origin of the hyobranchial apparatus in the Mexican axolotl (Ambystoma mexicanum)

Cardiac neural crest stem cells

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