Accessory atrioventricular muscle bundles. II. Cardiac conduction system in a human specimen with Wolff‐Parkinson‐White syndrome

Truex, Raymond C.; Bishof, J. K.; Downing, Daniel F.

doi:10.1002/ar.1091370403

“…If nonspecialized (working) myocardium remains at the AV junction, propagation of the electrical current through the heart is not normal and results in premature ventricular contractions, as seen in WolffParkinson-White syndrome. [2][3][4][5] In this issue of Circulation Research, Kim et al 6 present a detailed study using molecular markers to show the reorganization of the AV myocardium in formation of the AV junction in developing human heart. They have been able to follow certain portions of the AV canal myocardium using the spatial expression patterns of 2 markers, which this group has studied in heart development for many years.…”

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confidence: 99%

Getting to the Heart of Cardiac Morphogenesis

Kirby¹

2001

Circulation Research

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Does the subepicardial mesenchyme contribute myocardioblasts to the myocardium of the chick embryo heart? A quail-chick chimera study tracing the fate of the epicardial primordium

Mnner¹

1999

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Morris (J. Anat., 1976;121:47-64) proposed that the subepicardial mesenchyme might represent a continuing source of myocardioblasts during embryonic and fetal development. Recent studies have shown that the epicardium and subepicardial mesenchyme, and the coronary vasculature are all derived from a region of the pericardial wall, called the proepicardial serosa. In avian embryos, the cells from the proepicardial serosa colonize the heart via a secondary tissue bridge formed by attachment of proepicardial villi to the heart. In the present study, Morris's hypothesis was tested by tracing the fate of the proepicardial serosa. This was achieved by constructing quail-chick chimeras. The proepicardial serosa was transplanted from HH16/17 quail embryos to HH16/17 chick embryos (ED3). A new transplantation technique facilitated an orthotopic attachment of the quail proepicardial villi to the chicken heart, and prevented the attachment of the chicken proepicardial villi to the heart. The fate of the grafted quail cells was traced in chimeras from ED4 to ED18 with immunohistochemistry, using quail-specific antibodies (QCPN, QH-1). From ED4 onward, the transplant was connected to the dorsal heart wall via its proepicardial villi. Starting from the point of attachment of the quail proepicardial villi to the heart, the originally naked myocardium became almost completely covered by quail-derived epicardium, and quail mesenchymal cells populated the subepicardial, myocardial, and subendocardial layers including the av-endocardial cushions. Quail cells formed the endothelial and smooth muscles cells of the coronary vessels, and the perivascular and intramyocardial fibroblasts. Quail myocardial cells were never found in the subepicardial, myocardial, and subendocardial layers. This suggests that the subepicardial mesenchyme normally does not contribute a substantial number of myocardioblasts to the developing avian heart. The new transplantation technique presented facilitates the production of chimeric hearts in which the derivatives of the proepicardial serosa are almost completely of donor origin. This technique might be useful for future studies analyzing the role of certain genes in cardiac development by the creation of somatic transgenics.

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Does the subepicardial mesenchyme contribute myocardioblasts to the myocardium of the chick embryo heart? A quail‐chick chimera study tracing the fate of the epicardial primordium

Männer

¹

1999

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Morris (J. Anat., 1976;121:47-64) proposed that the subepicardial mesenchyme might represent a continuing source of myocardioblasts during embryonic and fetal development. Recent studies have shown that the epicardium and subepicardial mesenchyme, and the coronary vasculature are all derived from a region of the pericardial wall, called the proepicardial serosa. In avian embryos, the cells from the proepicardial serosa colonize the heart via a secondary tissue bridge formed by attachment of proepicardial villi to the heart. In the present study, Morris's hypothesis was tested by tracing the fate of the proepicardial serosa. This was achieved by constructing quail-chick chimeras. The proepicardial serosa was transplanted from HH16/17 quail embryos to HH16/17 chick embryos (ED3). A new transplantation technique facilitated an orthotopic attachment of the quail proepicardial villi to the chicken heart, and prevented the attachment of the chicken proepicardial villi to the heart. The fate of the grafted quail cells was traced in chimeras from ED4 to ED18 with immunohistochemistry, using quail-specific antibodies (QCPN, QH-1). From ED4 onward, the transplant was connected to the dorsal heart wall via its proepicardial villi. Starting from the point of attachment of the quail proepicardial villi to the heart, the originally naked myocardium became almost completely covered by quail-derived epicardium, and quail mesenchymal cells populated the subepicardial, myocardial, and subendocardial layers including the av-endocardial cushions. Quail cells formed the endothelial and smooth muscles cells of the coronary vessels, and the perivascular and intramyocardial fibroblasts. Quail myocardial cells were never found in the subepicardial, myocardial, and subendocardial layers. This suggests that the subepicardial mesenchyme normally does not contribute a substantial number of myocardioblasts to the developing avian heart. The new transplantation technique presented facilitates the production of chimeric hearts in which the derivatives of the proepicardial serosa are almost completely of donor origin. This technique might be useful for future studies analyzing the role of certain genes in cardiac development by the creation of somatic transgenics.

show abstract

Accessory atrioventricular muscle bundles. II. Cardiac conduction system in a human specimen with Wolff‐Parkinson‐White syndrome

Cited by 56 publications

References 7 publications

Getting to the Heart of Cardiac Morphogenesis

Getting to the Heart of Cardiac Morphogenesis

Does the subepicardial mesenchyme contribute myocardioblasts to the myocardium of the chick embryo heart? A quail-chick chimera study tracing the fate of the epicardial primordium

Does the subepicardial mesenchyme contribute myocardioblasts to the myocardium of the chick embryo heart? A quail‐chick chimera study tracing the fate of the epicardial primordium

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