Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-8-15
pubmed:abstractText
Insulin-like growth factor I (IGF-I) and transforming growth factor-beta1 (TGF-beta1) 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-beta1 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-beta1 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-beta1 inhibited basal DNA synthesis. TGF-beta1 and IGF-I each had similar but not additive effects to induce type I collagen. TGF-beta1 but not IGF-I potently stimulated expression of alpha-smooth muscle actin and stress fiber formation. IGF-I in combination with TGF-beta1 attenuated stress fiber formation without reducing alpha-smooth muscle actin expression. Stress fibers were not a prerequisite for increased collagen synthesis. TGF-beta1 upregulated IGF-I mRNA, which led us to examine the effects of IGF-I in cells previously activated by TGF-beta1 pretreatment. IGF-I potently stimulated proliferation of TGF-beta1-activated myofibroblasts without reversing activated fibrogenic phenotype. We conclude that TGF-beta1 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-beta1 and IGF-I, but they may act in concert to increase collagen deposition.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Actins, http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type I, http://linkedlifedata.com/resource/pubmed/chemical/DNA, http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor Binding..., http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor Binding..., http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I, http://linkedlifedata.com/resource/pubmed/chemical/Peptidoglycan, http://linkedlifedata.com/resource/pubmed/chemical/Polysaccharides, http://linkedlifedata.com/resource/pubmed/chemical/TGFB1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Tgfb1 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta, http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta1
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0193-1857
pubmed:author
pubmed:issnType
Print
pubmed:volume
283
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G809-18
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12181198-Actins, pubmed-meshheading:12181198-Animals, pubmed-meshheading:12181198-Cell Division, pubmed-meshheading:12181198-Cell Line, pubmed-meshheading:12181198-Collagen Type I, pubmed-meshheading:12181198-DNA, pubmed-meshheading:12181198-Enterocolitis, pubmed-meshheading:12181198-Fibroblasts, pubmed-meshheading:12181198-Fibrosis, pubmed-meshheading:12181198-Humans, pubmed-meshheading:12181198-Insulin-Like Growth Factor Binding Protein 3, pubmed-meshheading:12181198-Insulin-Like Growth Factor Binding Proteins, pubmed-meshheading:12181198-Insulin-Like Growth Factor I, pubmed-meshheading:12181198-Intestines, pubmed-meshheading:12181198-Muscle, Smooth, pubmed-meshheading:12181198-Peptidoglycan, pubmed-meshheading:12181198-Phenotype, pubmed-meshheading:12181198-Polysaccharides, pubmed-meshheading:12181198-Rats, pubmed-meshheading:12181198-Transforming Growth Factor beta, pubmed-meshheading:12181198-Transforming Growth Factor beta1
pubmed:year
2002
pubmed:articleTitle
IGF-I and TGF-beta1 have distinct effects on phenotype and proliferation of intestinal fibroblasts.
pubmed:affiliation
Department of Cell and Molecular Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7545, USA. jgs@med.unc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.