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  • Title: Induction of alpha-smooth muscle actin by transforming growth factor-beta 1 in quiescent human breast gland fibroblasts. Implications for myofibroblast generation in breast neoplasia.
    Author: Rønnov-Jessen L, Petersen OW.
    Journal: Lab Invest; 1993 Jun; 68(6):696-707. PubMed ID: 8515656.
    Abstract:
    BACKGROUND: By using a novel experimental system for the study of reactive fibroblast differentiation at the molecular level, we describe the induction of the alpha-isoform of smooth muscle actin by transforming growth factor-beta (TGF-beta 1) in human normal breast gland fibroblasts. EXPERIMENTAL DESIGN: The experimental system allowed fibroblasts to plate and remain quiescent and nonreactive but at the same time stay sensitive to environmental cues for more than 2 weeks after explantation. Most important, the biological activity of growth factors and cytokines could be studied without cells entering the cell cycle, thus serving as a model for stromal reactions with little cell turnover. RESULTS: By use of double-labeling immunocytochemistry, isoelectric focusing, two-dimensional gel electrophoresis, and fluorography, evidence is presented that the effect of TGF-beta 1 is dose-dependent with a maximal response above 80 pg/ml and a course of 6 days. No other growth factor/cytokine tested (platelet-derived growth factor, interleukin-1, insulin-like growth factor-1, acidic fibroblast growth factor, basic fibroblast growth factor, epidermal growth factor, and interferon-gamma) could induce alpha-smooth muscle actin on their own or potentiate the effect of TGF-beta 1. In an inhibitory assay, only basic fibroblast growth factor was found to prevent the action of TGF-beta 1. The relative contribution of TGF-beta 1-like activity to carcinoma cell induced alpha-smooth muscle actin in fibroblasts was deciphered using TGF-beta neutralizing antibodies and medium conditioned by two different breast carcinoma cell lines. Conditioned medium elicited a fibroblast response indistinguishable from that obtained with exogenously added TGF-beta 1, and indeed neutralization attributed the entire response to the sole effect of secreted TGF-beta 1-like activity. CONCLUSIONS: These results provide a strategy for the molecular characterization of epithelial-stromal interaction in breast neoplasia.
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