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Gamma interferon as an antifibrosis agent in skeletal muscle
Author(s) -
Foster William,
Li Yong,
Usas Arvydas,
Somogyi George,
Huard Johnny
Publication year - 2003
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1016/s0736-0266(03)00059-7
Subject(s) - skeletal muscle , fibrosis , decorin , regeneration (biology) , vimentin , cytokine , medicine , endocrinology , chemistry , microbiology and biotechnology , immunohistochemistry , anatomy , biology , proteoglycan , cartilage
Muscle injuries are a common problem in sports medicine. Skeletal muscle can regenerate itself, but the process is both slow and incomplete. Previously we and others have used growth factors to improve the regeneration of muscle, but the muscle healing was impeded by scar tissue formation. However, when we blocked the fibrosis process with decorin, an antifibrosis agent, we improved the muscle healing. Here we show that γinterferon (γINF)—a cytokine that inhibits the signaling of transforming growth factor β1 (TGFβ1), a fibrotic stimulator—reduces fibrosis formation and improves the healing of lacerated skeletal muscle. With γINF treatment, the growth rate of muscle‐derived fibroblasts was reduced and the level of fibrotic protein expression induced by TGFβ1 (including TGFβ1, vimentin, and α‐smooth muscle actin) was down‐regulated in vitro. In a mouse laceration model, the area of fibrosis decreased when γINF was injected at either 1 or 2 weeks after injury. More importantly, the injection of γINF at either 1 or 2 weeks post‐injury was found to improve muscle function in terms of both fast‐twitch and tetanic strength. This study demonstrates that γINF is a potent antifibrosis agent that can improve muscle healing after laceration injury. © 2003 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.