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Updated: Jun 5, 2026

A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Molecular atherectomy for restenosis
W Casscells1, D A Lappi, A Baird
1Texas Heart Institute and University of Texas Medical School, Houston, TX 77225-0345 USA.
Abstract:
Receptors for basic (b) and acidic (a) fibroblast growth factor (FGF) are upregulated in activated smooth muscle cells. These cells, which proliferate in response to bFGF, can thus be killed by a conjugate of bFGF and the ribosome-inactivating enzyme, saporin (which, by itself, does not enter the cells). Quiescent smooth muscle cells and other cells that have few FGF receptors are not killed. In vivo, bFGF-saporin transiently inhibits smooth muscle cell proliferation and neointimal accumulation after balloon injury to the rat carotid artery. Delivery of saporin, diagnostic imaging agents, or antisense oligodeoxynucleotides might be made even more selective by linking these substances to antibodies against the extracellular domains of the putative FGF receptor isoform specific for activated smooth muscle cells.
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