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A Novel Ex Ovo Banding Technique to Alter Intracardiac Hemodynamics in an Embryonic Chicken System
Published on: May 13, 2016
The endothelin-1 pathway and the development of cardiovascular defects in the haemodynamically challenged chicken
Bianca C W Groenendijk1, Sandra Stekelenburg-de Vos, Peter Vennemann
1Department of Anatomy and Embryology, Leiden University Medical Center, Leiden, The Netherlands.
Insights
Venous clipping in chicken embryos causes cardiovascular defects by affecting the endothelin-1 (ET-1) pathway. This study shows ET-1 and antagonists disrupt embryonic heart function and morphology, impacting development.
Area of Science:
- Developmental biology
- Cardiovascular research
- Embryology
Background:
- Venous clipping in chicken embryos causes cardiovascular malformations.
- These defects resemble those seen in endothelin-1 (ET-1) pathway knockout mice.
- Previous studies show decreased cardiac ET-1 expression and disturbed ventricular filling post-clipping.
Purpose of the Study:
- To investigate the role of the endothelin-1 (ET-1) pathway in cardiovascular defects induced by venous clipping.
- To determine the effects of ET-1 and its receptor antagonists on embryonic cardiovascular function and morphology.
Main Methods:
- Infusion of ET-1 and receptor antagonists (BQ-123, BQ-788, PD145065) into HH18 chicken embryos.
- Assessment of immediate hemodynamic effects using Doppler and micro-particle image velocimetry.
- Analysis of ventricular diastolic filling at HH24 and cardiovascular morphology at HH35.
Main Results:
- ET-1 and antagonists induced hemodynamic changes at HH18.
- A reduced passive ventricular filling component and increased active filling were observed at HH24.
- Thinner ventricular myocardium was noted in 42% of experimental embryos.
Conclusions:
- Cardiovascular malformations after venous clipping result from combined hemodynamic changes and altered gene expression, including the endothelin pathway.
- The endothelin-1 pathway is implicated in the development of functional and morphological cardiovascular defects post-venous clipping.
Background/Aims:
Ligating the right lateral vitelline vein of chicken embryos (venous clip) results in cardiovascular malformations. These abnormalities are similar to malformations observed in knockout mice studies of components of the endothelin-1 (ET-1)/endothelin-converting enzyme-1/endothelin-A receptor pathway. In previous studies we demonstrated that cardiac ET-1 expression is decreased 3 h after clipping, and ventricular diastolic filling is disturbed after 2 days. Therefore, we hypothesise that ET-1-related processes are involved in the development of functional and morphological cardiovascular defects after venous clip.
Methods:
In this study, ET-1 and endothelin receptor antagonists (BQ-123, BQ-788 and PD145065) were infused into the HH18 embryonic circulation. Immediate haemodynamic effects on the embryonic heart and extra-embryonic vitelline veins were examined by Doppler and micro-particle image velocimetry. Ventricular diastolic filling characteristics were studied at HH24, followed by cardiovascular morphologic investigation (HH35).
Results:
ET-1 and its receptor antagonists induced haemodynamic effects at HH18. At HH24, a reduced diastolic ventricular passive filling component was demonstrated, which was compensated by an increased active filling component. Thinner ventricular myocardium was shown in 42% of experimental embryos.
Conclusion:
We conclude that cardiovascular malformations after venous clipping arise from a combination of haemodynamic changes and altered gene expression patterns and levels, including those of the endothelin pathway.
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