{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T11:14:57Z","timestamp":1789470897396,"version":"build-2803163510"},"reference-count":45,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2017,2,23]],"date-time":"2017-02-23T00:00:00Z","timestamp":1487808000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Orthopaedic Research"],"published-print":{"date-parts":[[2017,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:label\/><jats:p>Myofibroblasts (MFs), a contractile subset of fibroblasts, play a pivotal role in physiological wound healing and in the development of many fibroconnective disorders. The complex cytokine network regulating the function of MFs in joint stiffness is still poorly understood. In this in vitro study, we investigated the effect of the cytokine Interferon\u2010gamma (IFN\u2010\u03b3) on MFs isolated from human joint capsules. MFs were cultivated either in the presence of increasing concentrations of IFN\u2010\u03b3 alone or in combination with IFN\u2010\u03b3 neutralizing antibodies. Cell viability, cytotoxicity, apoptosis, and mRNA gene expression of the MF markers alpha\u2010smooth muscle actin (\u03b1\u2010SMA) and collagen type I were analyzed in MF cultures. Contraction potential was analyzed in an established collagen gel contraction assay simulating the extracellular matrix. Using immunofluorescence staining, we could verify that MFs express IFN\u2010\u03b3\u2010receptor (R)\u20101 on their membrane. IFN\u2010\u03b3 decreased MF viability and significantly elevated the apoptosis rate in a dose\u2010dependent manner. IFN\u2010\u03b3 down\u2010regulated \u03b1\u2010SMA and collagen type I mRNA expression which was associated with a diminished MF mediated contraction of the gel matrices. These effects were suppressed by simultaneous treatment of cells with a neutralizing IFN\u2010\u03b3 antibody. Our experiments confirm the hypothesis that the cytokine IFN\u2010\u03b3 is a crucial component of the regulatory network of capsule MFs. IFN\u2010\u03b3 notably influences the ability of MFs to contract collagen matrices by suppressing \u03b1\u2010SMA gene expression. IFN\u2010\u03b3 is toxic for MFs in high concentrations and may negatively regulate the number of pro\u2010fibrotic MFs during the healing process via induction of cell apoptosis. \u00a9 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. 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