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Am J Physiol Gastrointest Liver Physiol 283: G809-G818, 2002. First published April 24, 2002; doi:10.1152/ajpgi.00057.2002
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Vol. 283, Issue 3, G809-G818, September 2002

IGF-I and TGF-beta 1 have distinct effects on phenotype and proliferation of intestinal fibroblasts

James G. Simmons1, Jolanta B. Pucilowska1,2, Temitope O. Keku2, and P. Kay Lund1,2

1 Department of Cell and Molecular Physiology and 2 Center for Gastrointestinal Biology and Disease, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7545

Insulin-like growth factor I (IGF-I) and transforming growth factor-beta 1 (TGF-beta 1) are upregulated in myofibroblasts at sites of fibrosis in experimental enterocolitis and in Crohn's disease (CD). We compared the sites of expression of IGF-I and TGF-beta 1 in a rat peptidoglycan-polysaccharide (PG-PS) model of chronic granulomatous enterocolitis and fibrosis. We used the human colonic CCD-18Co fibroblast/myofibroblast cell line to test the hypothesis that TGF-beta 1 and IGF-I interact to regulate proliferation, collagen synthesis, and activated phenotype typified by expression of alpha -smooth muscle actin and organization into stress fibers. IGF-I potently stimulated while TGF-beta 1 inhibited basal DNA synthesis. TGF-beta 1 and IGF-I each had similar but not additive effects to induce type I collagen. TGF-beta 1 but not IGF-I potently stimulated expression of alpha -smooth muscle actin and stress fiber formation. IGF-I in combination with TGF-beta 1 attenuated stress fiber formation without reducing alpha -smooth muscle actin expression. Stress fibers were not a prerequisite for increased collagen synthesis. TGF-beta 1 upregulated IGF-I mRNA, which led us to examine the effects of IGF-I in cells previously activated by TGF-beta 1 pretreatment. IGF-I potently stimulated proliferation of TGF-beta 1-activated myofibroblasts without reversing activated fibrogenic phenotype. We conclude that TGF-beta 1 and IGF-I both stimulate type I collagen synthesis but have differential effects on activated phenotype and proliferation. We propose that during intestinal inflammation, regulation of activated phenotype and proliferation may require sequential actions of TGF-beta 1 and IGF-I, but they may act in concert to increase collagen deposition.

Crohn's disease; alpha -smooth muscle actin; fibrosis


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