Resolution of defective dorsal aortae patterning in Sema3E-deficient mice occurs via angiogenic remodeling

What is it about?

In this study, we examine how semaphorin signaling from the extra-vascular environment influences the migration and patterning of early blood vessels. In particular, we examine how the dorsal aorta forms in mouse. Past studies have shown that it arises from two parallel tubes that arise parallel to the embryonic midline. We find here that Sema3E is expressed between these early tubes and is required for their normal cylindrical shape. Sema3E is known to repulse cells via its interaction with its receptor located on endothelial cells (PlexinD1). It is considered a guidance cue, because of this ability. Upon the absence of this molecule, the aortae coalesce into abnormal plexuses (or connected network of vessels) instead of large unbranched tubes.

Featured Image

Why is it important?

These findings are important as they identify a molecule that affects endothelial cell migration and behavior. It is required for a specific blood vessel to form in a certain way. When it is gone, the shape of the vessel is disrupted. Interestingly, we find that other repulsive molecules also influence early vessel formation. Additional guidance cues are found at the midline, preventing errant migration of endothelial cells in this region, regardless of presence or absence of Sema3E. Finding why vessels expand into tissues, or not, due to presence or absence of cues will help us learn how best to manipulate blood vessel growth both in anti- or pro-angiogenic therapies, such as in cancer, diabetic retinopathies or bioengineering of replacement tissues.