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Articles in PresS, published online ahead of print April 24, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00057.2002
Submitted on February 11, 2002
Accepted on April 15, 2002
1 Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, NC, USA
2 Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, NC, USA; Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, NC, USA
3 Center for Gastrointestinal Biology and Disease, University of North Carolina, Chapel Hill, NC, USA
* To whom correspondence should be addressed. E-mail: jgs{at}med.unc.edu.
Insulin-like growth factor I (IGF-I) and transforming growth factor-ß1 (TGF-ß) are up-regulated 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-ß 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-ß1 and IGF-I interact to regulate proliferation, collagen synthesis and activated phenotype typified by expression of smooth muscle 
actin (SM-actin) and organization into stress fibers. IGF-I potently stimulated while TGF-ß1 inhibited basal DNA synthesis. TGF-ß1 and IGF-I each had a similar but not additive effects to induce type I collagen. TGF-ß1 but not IGF-I potently stimulated expression of SM-actin and stress fiber formation. IGF-I in combination with TGF-ß1 attenuated stress fiber formation without reducing SM-actin expression. Stress fibers were not a prerequisite for increased collagen synthesis. TGF-ß1 up-regulated IGF-I mRNA which led us to examine the effects of IGF-I in cells previously activated by TGF-ß1 pretreatment. IGF-I potently stimulated proliferation of TGF-ß1-activated myofibroblasts without reversing activated, fibrogenic phenotype. We conclude that TGF-ß1 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-ß1 and IGF-I, but they may act in concert to increase collagen deposition.
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