(Circulation. 1995;91:2699-2702.)
© 1995 American Heart Association, Inc.
Articles |
From the Cardiology Division, University of Texas Medical School at Houston; Hermann Hospital; and Texas Heart Institute (Houston).
Correspondence to Ward Casscells, MD, Texas Heart Institute, MC 2-255, PO Box 20345, Houston, TX 77225-0345.
| Introduction |
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50%, although the 4-week end point is too
early to be certain. Recently, Callow et al2 reported
equally dramatic effects using twice-weekly intravenous doses of 100
µg in the rabbit. Although no toxicity was described in the rabbit
studies, the present report by Asahara and colleagues suggests that
a single local administration is efficacious, eliminating concerns
about other potential in vivo effects of VEGF, including
vasorelaxation3 and increased vascular
permeability.4 These outcomes were by no means guaranteed, since there was no previous evidence that VEGF played a role in this process. VEGF, a glycoprotein that is mitogenic for endothelial cells and angiogenic in vivo, is known to be expressed in ischemic and hypoxic myocytes5 6 and tumor cells (and indeed, the VEGF and erythropoietin genes have similar hypoxia-responsive regulatory regions7 ), but injured arteries are not hypoxic. VEGF is made by smooth muscle cells, and it may prove to be upregulated after balloon injury, since in other cells its expression is induced by protein kinase C and by tissue factor,8 which are activated after balloon injury.
These studies are also noteworthy for the magnitude of the effects,
which contrast with reports that growth factors only marginally enhance
dermal wound healing in normal
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