Key result
Aortic injury in rats induced expression of PDGF-A and -B chains and PDGF alpha-receptor in endothelial cells at the wound edge, suggesting a paracrine role for endothelial PDGF in SMC migration.
Endothelial expression of PDGF-B after injury may play a paracrine role in smooth muscle cell migration into the intima.
Should not alter clinical vascular care; leaves open endothelial PDGF as a paracrine driver of human intimal hyperplasia.
In situ hybridization and immunostaining were used to study the time course of expression for platelet-derived growth factor (PDGF) ligands and receptors in endothelium of the rat aorta after injury. The PDGF-A and -B chains were expressed in endothelial cells at the wound edge within 4 h after injury, but no expression was detectable in uninjured endothelium. PDGF alpha-receptor was expressed in a pattern similar to the PDGF-A chain, while expression of PDGF beta-receptor was not detected at any time. Expression of the PDGF-B chain remained elevated in endothelial cells at the leading edge even at later measurements when these cells had stopped replicating. Smooth muscle cells (SMCs), which are absent from the intima of the normal aorta and are known to express PDGF beta-receptors, were predominantly found to migrate into the intima near the endothelial leading edge where PDGF-B was expressed. These data suggest a paracrine role for endothelial PDGF in SMC migration.
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Volkhard Lindner (2008) studied Aortic injury. Aortic injury vs. Uninjured endothelium was evaluated on Expression of PDGF ligands and receptors. Aortic injury in rats induced expression of PDGF-A and -B chains and PDGF alpha-receptor in endothelial cells at the wound edge, suggesting a paracrine role for endothelial PDGF in SMC migration.
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