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Updated: Mar 28, 2026
Analysis of Coronary Vessels in Cleared Embryonic Hearts
Published on: December 7, 2016
Coronary stem development in wild-type and Tbx1 null mouse hearts
Magali Théveniau-Ruissy1, José-Maria Pérez-Pomares2,3, Pauline Parisot1
1Aix-Marseille University, CNRS, IBDM UMR 7288, Marseille, France.
Insights
A periarterial vascular plexus aids coronary artery stem development by connecting aortic and ventricular vessels. Tbx1 influences coronary artery patterning, offering insights into congenital heart defects.
Area of Science:
- Developmental biology
- Cardiovascular research
- Genetics
Background:
- Coronary artery (CA) stems are crucial for heart blood supply.
- Defects in CA development can lead to sudden cardiac death.
- Tbx1 gene mutations are linked to abnormal CA development.
Purpose of the Study:
- Investigate the developmental mechanisms of coronary artery stems.
- Clarify the role of Tbx1 in CA stem formation and patterning.
- Understand the origin of the periarterial vascular plexus.
Main Methods:
- Genetic lineage tracing in mouse embryos.
- Immunohistochemistry and fluorescent tracer injections.
- Avian embryo transplantation experiments.
Main Results:
- Limited aortic endothelium outgrowth contributes to CA stems.
- A periarterial vascular plexus forms early in CA stem development.
- Tbx1 is essential for CA stem patterning, not timing, with specific myocardial expression.
Conclusions:
- A periarterial plexus connects aortic endothelium to the ventricular plexus during CA stem development.
- Molecular asymmetries between left and right CA stems are identified.
- Findings provide insights into the causes of CA patterning defects.
Background:
Coronary artery (CA) stems connect the ventricular coronary tree with the aorta. Defects in proximal CA patterning are a cause of sudden cardiac death. In mice lacking Tbx1, common arterial trunk is associated with an abnormal trajectory of the proximal left CA. Here we investigate CA stem development in wild-type and Tbx1 null embryos.
Results:
Genetic lineage tracing reveals that limited outgrowth of aortic endothelium contributes to proximal CA stems. Immunohistochemistry and fluorescent tracer injections identify a periarterial vascular plexus present at the onset of CA stem development. Transplantation experiments in avian embryos indicate that the periarterial plexus originates in mesenchyme distal to the outflow tract. Tbx1 is required for the patterning but not timing of CA stem development and a Tbx1 reporter allele is expressed in myocardium adjacent to the left but not right CA stem. This expression domain is maintained in Sema3c(-/-) hearts with a common arterial trunk and leftward positioned CA. Ectopic myocardial differentiation is observed on the left side of the Tbx1(-/-) common arterial trunk.
Conclusions:
A periarterial plexus bridges limited outgrowth of the aortic endothelium with the ventricular plexus during CA stem development. Molecular differences associated with left and right CA stems provide new insights into the etiology of CA patterning defects.
