Other MVs evolve into vascular malformation (VM) by retaining their large size and acquiring a smooth muscle-cell coating.
Unlike MV and GMP, these last vessels have acquired a complete and often multilayered pericyte or smooth muscle-cell coat, and lose detectable VEGFR-2 expression (unpublished data).
Moreover, unlike MVs and GMPs, VMs persist indefinitely in a low VEGF-A environment, although it is quite possible that their lining endothelium is maintained by VEGF-A secreted by their smooth muscle-cell coat.
CD44 has been demonstrated to be critical for keratinocyte, fibroblast, and smooth muscle cell HA coat formation [ 32– 340 42] 42] and both CD44 and RHAMM [ 12, 14, 61] have recently been implicated in the binding of HA to tumor cells and fibroblasts.
On the other hand, aberrant structures induced by high VEGF always regressed after TRAP treatment, but they lacked pericytes and were coated by smooth muscle cells instead.
The higher vulnerability of veins in comparison to arteries could be explained by the lower numbers of smooth muscle cells and pericytes coating the vessels, as it is likely that the transition to VEGF-independence is based on a maturing relationship between endothelial cells and pericytes [26].
These controls are what determines a cell's future: whether it grows into a heart cell, a muscle cell, or perhaps a brain cell.
Vascular Smooth Muscle Cell.
In chicken pectoral muscle cell cultures, FST enhanced muscle cell development (Link and Nishi 1997).
EC, endothelial cell; VSMC, vascular smooth muscle cell.
