Recombinant fibroblast growth factor-1 promotes intimal hyperplasia and angiogenesis in arteries in vivo

Elizabeth G. Nabel, Zhi Yong Yang, Gregory Plautz, Reza Forough, Xi Zhan, Christian C. Haudenschild, Thomas Maciag, Gary J. Nabel

Research output: Contribution to journalArticlepeer-review

317 Scopus citations


THE prototype members of the heparin-binding fibroblast growth factor (FGF) family1-6, acidic FGF (FGF-1) and basic FGF (FGF-2), are among the growth factors that act directly on vascular cells to induce endothelial cell growth and angiogenesis. In vivo, the role of the FGF prototypes in vascular pathology has been difficult to determine. We report here the introduction, by direct gene transfer into porcine arteries, of a eukaryotic expression vector encoding a secreted form of FGF-1. This somatic transgenic model defines gene function in the arterial wall in vivo. FGF-1 expression induced intimal thickening in porcine arteries 21 days after gene transfer, in contrast to control arteries transduced with an Escherichia coli β-galactosidase gene. Where there was substantial intimai hyperplasia, neocapillary formation was detected in the expanded intima. These findings suggest that FGF-1 induces intimai hyperplasia in the arterial wall in vivo and, through its ability to stimulate angiogenesis in the neointima, FGF-1 could stimulate neovascularization of atherosclerotic plaques. Potentially, gene transfer of FGF-1 could also be used as a genetic intervention to improve blood flow to ischaemic tissues in selected clinical settings.

Original languageEnglish (US)
Pages (from-to)844-846
Number of pages3
Issue number6423
StatePublished - 1993
Externally publishedYes

ASJC Scopus subject areas

  • General


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