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Identification of FGF-1-Inducible Genes by Differential Display

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Cardiovascular Disease

Abstract

Endothelial cells and smooth muscle cells, the most abundant cell types in the blood vessel wall, normally have a low replication rate in the adult animal. However, endothelial cell proliferation and concomitant neovascularization is associated with tumor growth and the pathogenesis of numerous angiogenesis-dependent diseases.1 Also, accelerated smooth muscle cell replication plays a central role in atherogenesis,2 vascular graft stenosis,3 and restenosis of vessels following angioplasty or atherectomy.4 Fibroblast growth factor (FGF)-1 and FGF-2, also commonly known as acidic and basic FGF, respectively, are two of the polypeptide mitogens that are likely to be important mediators of vascular cell growth in vivo. They are both potent angiogenic factors5,6 and smooth muscle cell mitogens.7,8 They are expressed by vessel wall cells9,10 and by monocyte-derived macrophages within human atheroma.9,10 FGF-2 has also been detected in human platelets11 and T lymphocytes.12 Direct evidence for the involvement of FGF-2 in rat balloon injury-induced medial smooth muscle cell proliferation was reported by Lindner and Reidy.13 Therefore, it is possible that inhibition of FGF expression or action may be of therapeutic benefit in the treatment of human cardiovascular disease. One strategy that may prove effective for inhibition of FGF mitogenic activity is to interrupt the FGF intracellular signaling pathway. In this review, we describe our approach to identify proteins that are involved in FGF-1 mitogenic signal transduction and thus potential targets for therapeutic intervention.

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Winkles, J.A., Donohue, P.J., Hsu, D.K.W., Guo, Y., Alberts, G.F., Peifley, K.A. (1995). Identification of FGF-1-Inducible Genes by Differential Display. In: Gallo, L.L. (eds) Cardiovascular Disease. GWUMC Department of Biochemistry Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1959-1_15

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  • DOI: https://doi.org/10.1007/978-1-4615-1959-1_15

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