PDGF-BB AND IGF-I USE DIFFERENT SIGNALING PATHWAYS TO INDUCE FIBRONECTIN SYNTHESIS IN CULTURED RAT THORACIC AORTIC SMOOTH MUSCLE CELLS

Authors

  • Chu S. Lo Ph.D.

    Corresponding author
    1. Department of Physiology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD, 20814, U.S.A.
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To whom correspondence should be addressed: Chu S. Lo, Ph.D. Department of Physiology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, U.S.A. E-mail: CLO@USUHS.Mil

Abstract

Fibronectin, an extracellular matrix protein, acts as an early signal in initiating cell proliferation. Results have indicated that platelet-derived growth factor BB (PDGF-BB) and insulin-like growth factor-I (IGF-I) both enhance fibronectin gene expression. Genistein inhibits PDGF-BB-induced fibronectin levels without inhibiting IGF-I-induced fibronectin levels. It indicates that PDGF-BB and IGF-I utilize separate signaling pathways to induce the synthesis of fibronectin.

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