{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T09:33:44Z","timestamp":1789205624927,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2015,10,14]],"date-time":"2015-10-14T00:00:00Z","timestamp":1444780800000},"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":[[2016,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:label\/><jats:p>The etiology of intervertebral disc (IVD) degeneration is closely related to apoptosis and extracellular matrix degradation in nucleus pulposus (NP) cells. These defects in NP cells are induced by excessive external stressors such as reactive oxygen species (ROS) and inflammatory cytokines. Recently, hepatocyte growth factor (HGF) has been shown to repair damage in various diseases through anti\u2010apoptotic and anti\u2010inflammatory activity. In this study, we investigated the effects of HGF on NP cell abnormality caused by ROS and inflammatory cytokines by using primary NP cells isolated from rabbit IVD. HGF significantly enhanced the proliferation of NP cells. Apoptosis of NP cells induced by H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> or TNF\u2010\u03b1 was significantly inhibited by HGF. Induction of mRNA expression of the inflammation mediators cyclooxygenase\u20102 and matrix metalloproteinase\u20103 and \u20109 by TNF\u2010\u03b1 was significantly suppressed by HGF treatment. Expression of c\u2010Met, a specific receptor for HGF, was confirmed in NP cells and was increased by TNF\u2010\u03b1, suggesting that inflammatory cytokines increase sensitivity to HGF. These findings demonstrate that activation of HGF\/c\u2010Met signaling suppresses damage caused by ROS and inflammation in NP cells through multiple pathways. We further suggest the clinical potential of HGF for counteracting IVD degradation involved in NP cell abnormalities. \u00a9 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. 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