The study findings appear in the June 15 issue of the journal Blood.
Blood vessel formation, or angiogenesis, is an integral part of normal organ development and function. It also contributes to abnormal conditions, particularly tumor formation and growth.
Angiogenesis begins with the establishment of an intricately branched rudimentary network called the vascular plexus, which is assembled from blood vessel precursor cells. This is followed by increased cell division of specific cells, endothelial cells that make up the lining of blood vessels.
These cells then sprout and migrate away from the parent vessel, and the sprouts ultimately connect with each other, allowing the vessel network to expand. This process is called sprouting angiogenesis.
"It is very important to understand the sprouting process, because it occurs any time there is angiogenesis, whether for helpful reasons, such as wound healing, or in the context of pathology, such as cancer," said Dr. Victoria L. Bautch, who is a member of the School of Medicine's Carolina Cardiovascular Biology Center and a professor of biology at the university. Angiogenesis is coordinated by the actions of a number of proteins, and one of the most critical regulators of this process is the protein Vascular Endothelial Growth Factor-A, or VEGFA, said Bautch. Sprouting angiogenesis occurs as a result of the interactions of VEGFA with two cell receptor molecules, VEGFR1 (also called flt-1) and VEGFR2 (also called flk-1), she added.
While flk-1 is thought to promote endothelial cell division, the exact functions of flt-1 are poorly understood and have been difficult to uncover until now, said Bautch.