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Ablation of the secondary heart field leads to tetralogy of Fallot and pulmonary atresia.

Publication ,  Journal Article
Ward, C; Stadt, H; Hutson, M; Kirby, ML
Published in: Dev Biol
August 1, 2005

Recent studies in chick and mouse embryos have identified a previously unrecognized secondary heart field (SHF), located in the ventral midline splanchnic mesenchyme, which provides additional myocardial cells to the outflow tract as the heart tube lengthens during cardiac looping. In order to further delineate the contribution of this secondary myocardium to outflow development, we labeled the right SHF of Hamburger-Hamilton (HH) stage 14 chick embryos via microinjection of DiI/rhodamine and followed the fluorescently labeled cells over a 96-h time period. These experiments confirmed the movement of the SHF into the outflow and its spiraling migration distally, with the right side of the SHF contributing to the left side of the outflow. In contrast, when the right SHF was labeled at HH18, the fluorescence was limited to the caudal wall of the lengthening aortic sac. We then injected a combination of DiI and neutral red dye, and ablated the SHF in HH14 or 18 chick embryos. Embryos were allowed to develop until day 9, and harvested for assessment of outflow alignment. Of the embryos ablated at HH14, 76% demonstrated cardiac defects including overriding aorta and pulmonary atresia, while none of the sham-operated controls were affected. In addition, the more severely affected embryos demonstrated coronary artery anomalies. The embryos ablated at HH18 also manifested coronary artery anomalies but maintained normal outflow alignment. Therefore, the myocardium added to the outflow by the SHF at earlier stages is required for the elongation and appropriate alignment of the outflow tract. However, at later stages, the SHF contributes to the smooth muscle component of the outflow vessels above the pulmonary and aortic valves which is important for the development of the coronary artery stems. This work suggests a role for the SHF in a subset of congenital heart defects that have overriding aorta and coronary artery anomalies, such as tetralogy of Fallot and double outlet right ventricle.

Duke Scholars

Published In

Dev Biol

DOI

ISSN

0012-1606

Publication Date

August 1, 2005

Volume

284

Issue

1

Start / End Page

72 / 83

Location

United States

Related Subject Headings

  • Tetralogy of Fallot
  • Pulmonary Atresia
  • Myocardium
  • Morphogenesis
  • Models, Biological
  • In Situ Hybridization
  • Immunohistochemistry
  • Heart
  • Fluorescent Dyes
  • Developmental Biology
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Ward, C., Stadt, H., Hutson, M., & Kirby, M. L. (2005). Ablation of the secondary heart field leads to tetralogy of Fallot and pulmonary atresia. Dev Biol, 284(1), 72–83. https://doi.org/10.1016/j.ydbio.2005.05.003
Ward, Cary, Harriett Stadt, Mary Hutson, and Margaret L. Kirby. “Ablation of the secondary heart field leads to tetralogy of Fallot and pulmonary atresia.Dev Biol 284, no. 1 (August 1, 2005): 72–83. https://doi.org/10.1016/j.ydbio.2005.05.003.
Ward C, Stadt H, Hutson M, Kirby ML. Ablation of the secondary heart field leads to tetralogy of Fallot and pulmonary atresia. Dev Biol. 2005 Aug 1;284(1):72–83.
Ward, Cary, et al. “Ablation of the secondary heart field leads to tetralogy of Fallot and pulmonary atresia.Dev Biol, vol. 284, no. 1, Aug. 2005, pp. 72–83. Pubmed, doi:10.1016/j.ydbio.2005.05.003.
Ward C, Stadt H, Hutson M, Kirby ML. Ablation of the secondary heart field leads to tetralogy of Fallot and pulmonary atresia. Dev Biol. 2005 Aug 1;284(1):72–83.
Journal cover image

Published In

Dev Biol

DOI

ISSN

0012-1606

Publication Date

August 1, 2005

Volume

284

Issue

1

Start / End Page

72 / 83

Location

United States

Related Subject Headings

  • Tetralogy of Fallot
  • Pulmonary Atresia
  • Myocardium
  • Morphogenesis
  • Models, Biological
  • In Situ Hybridization
  • Immunohistochemistry
  • Heart
  • Fluorescent Dyes
  • Developmental Biology