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    Follistatin attenuates radiation-induced fibrosis in a murine model

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    Author
    Forrester, HB; de Kretser, DM; Leong, T; Hagekyriakou, J; Sprung, CN
    Date
    2017-03-16
    Source Title
    PLoS One
    Publisher
    PUBLIC LIBRARY SCIENCE
    University of Melbourne Author/s
    Leong, Trevor
    Affiliation
    Clinical Pathology
    Metadata
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    Document Type
    Journal Article
    Citations
    Forrester, H. B., de Kretser, D. M., Leong, T., Hagekyriakou, J. & Sprung, C. N. (2017). Follistatin attenuates radiation-induced fibrosis in a murine model. PLOS ONE, 12 (3), https://doi.org/10.1371/journal.pone.0173788.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258354
    DOI
    10.1371/journal.pone.0173788
    Abstract
    PURPOSE: Fibrosis can be a disabling, severe side effect of radiotherapy that can occur in patients, and for which there is currently no effective treatment. The activins, proteins which are members of the TGFβ superfamily, have a major role in stimulating the inflammatory response and subsequent fibrosis. Follistatin is an endogenous protein that binds the activins virtually irreversibly and inhibits their actions. These studies test if follistatin can attenuate the fibrotic response using a murine model of radiation-induced fibrosis. EXPERIMENTAL DESIGN: C57BL/6 mice were subcutaneously injected with follistatin 24 hours prior to irradiation. Mice were irradiated in a 10 x 10 mm square area of the right hind leg with 35 Gy and were given follistatin 24 hours before radiation and three times a week for six months following. Leg extension was measured, and tissue was collected for histological and molecular analysis to evaluate the progression of the radiation-induced fibrosis. RESULTS: Leg extension was improved in follistatin treated mice compared to vehicle treated mice at six months after irradiation. Also, epidermal thickness and cell nucleus area of keratinocytes were decreased by the follistatin treatment compared to the cells in irradiated skin of control mice. Finally, the gene expression of transforming growth factor β1 (Tgfb1), and smooth muscle actin (Acta2) were decreased in the irradiated skin and Acta2 and inhibin βA subunit (Inhba) were decreased in the irradiated muscle of the follistatin treated mice. CONCLUSIONS: Follistatin attenuated the radiation-induced fibrotic response in irradiated mice. These studies provide the data to support further investigation of the use of follistatin to reduce radiation-induced fibrosis in patients undergoing radiotherapy for cancer.

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