Title: Sox4 is involved in osteoarthritic cartilage deterioration through induction of ADAMTS4 and ADAMTS5
Abstract: The FASEB JournalVolume 33, Issue 1 p. 619-630 ResearchFree to Read Sox4 is involved in osteoarthritic cartilage deterioration through induction of ADAMTS4 and ADAMTS5 Yoshifumi Takahata, Corresponding Author Yoshifumi Takahata [email protected] Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan Correspondence: Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita, Osaka 565-0871, Japan. E-mail: [email protected]Search for more papers by this authorEriko Nakamura, Eriko Nakamura Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorKenji Hata, Kenji Hata Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorMakoto Wakabayashi, Makoto Wakabayashi Laboratory for Advanced Drug Discovery Pharmaceuticals Research Center, Asahi Kasei Pharma Corporation, Izunokuni, JapanSearch for more papers by this authorTomohiko Murakami, Tomohiko Murakami Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorKanta Wakamori, Kanta Wakamori Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorHiroshi Yoshikawa, Hiroshi Yoshikawa Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorAkio Matsuda, Akio Matsuda Laboratory for Advanced Drug Discovery Pharmaceuticals Research Center, Asahi Kasei Pharma Corporation, Izunokuni, JapanSearch for more papers by this authorNaoshi Fukui, Naoshi Fukui Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Tokyo, Japan Clinical Research Center, National Hospital Organization Sagamihara Hospital, Sagamihara, JapanSearch for more papers by this authorRiko Nishimura, Riko Nishimura Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this author Yoshifumi Takahata, Corresponding Author Yoshifumi Takahata [email protected] Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan Correspondence: Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita, Osaka 565-0871, Japan. E-mail: [email protected]Search for more papers by this authorEriko Nakamura, Eriko Nakamura Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorKenji Hata, Kenji Hata Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorMakoto Wakabayashi, Makoto Wakabayashi Laboratory for Advanced Drug Discovery Pharmaceuticals Research Center, Asahi Kasei Pharma Corporation, Izunokuni, JapanSearch for more papers by this authorTomohiko Murakami, Tomohiko Murakami Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorKanta Wakamori, Kanta Wakamori Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorHiroshi Yoshikawa, Hiroshi Yoshikawa Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this authorAkio Matsuda, Akio Matsuda Laboratory for Advanced Drug Discovery Pharmaceuticals Research Center, Asahi Kasei Pharma Corporation, Izunokuni, JapanSearch for more papers by this authorNaoshi Fukui, Naoshi Fukui Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Tokyo, Japan Clinical Research Center, National Hospital Organization Sagamihara Hospital, Sagamihara, JapanSearch for more papers by this authorRiko Nishimura, Riko Nishimura Department of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, JapanSearch for more papers by this author First published: 17 July 2018 https://doi.org/10.1096/fj.201800259RCitations: 2 This article includes supplemental data. Please visit http://www.fasebj.org to obtain this information. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL ABSTRACT Osteoarthritis is a common disease in joint cartilages. Because the molecular pathogenesis of osteoarthritis remains elusive, early diagnostic markers and effective therapeutic agents have not been developed. To understand the molecular mechanisms, we attempted to identify transcription factors involved in the onset of osteoarthritis. Microarray analysis of mouse articular cartilage cells indicated that retinoic acid, a destructive stimulus in articular cartilage, up-regulated expression of sex-determining region Y-box (Sox)4, a SoxC family transcription factor, together with increases in Adamts4 and Adamts5, both of which are aggrecanases of articular cartilages. Overexpression of Sox4 induced a disintegrin-like and metallopeptidase with thrombospondin type 4 and 5 motif (ADAMTS4 and ADAMTS5, respectively) expression in chondrogenic cell lines C3H10T1/2 and SW1353. In addition, luciferase reporter and chromatin immunoprecipitation assays showed that Sox4 up-regulated ADAMTS4 and Adamts5 gene promoter activities by binding to their gene promoters. Another SoxC family member, Sox11, evoked similar effects. To evaluate the roles of Sox4 and Sox11 in articular cartilage destruction, we performed organ culture experiments using mouse femoral head cartilages. Sox4 and Sox11 adenovirus infections caused destruction of articular cartilage associated with increased Adamts5 expression. Finally, SOX4 and SOX11 mRNA expression was increased in cartilage of patients with osteoarthritis compared with nonosteoarthritic subjects. Thus, Sox4, and presumably Sox11, are involved in osteoarthritis onset by up-regulating ADAMTS4 and ADAMTS5.—Takahata, Y., Nakamura, E., Hata, K., Wakabayashi, M., Murakami, T., Wakamori, K., Yoshikawa, H., Matsuda, A., Fukui, N., Nishimura, R. Sox4 is involved in osteoarthritic cartilage deterioration through induction of ADAMTS4 and ADAMTS5. FASEB J. 33, 619–630 (2019). www.fasebj.org Citing Literature Supporting Information Filename Description fsb2fj201800259r-sup-0001.docxapplication/docx, 86.8 KB Supplementary Material fsb2fj201800259r-sup-0002.aiapplication/ai, 72.7 MB Supplementary Material fsb2fj201800259r-sup-0003.aiapplication/ai, 1.6 MB Supplementary Material fsb2fj201800259r-sup-0004.aiapplication/ai, 1.7 MB Supplementary Material Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. Volume33, Issue1January 2019Pages 619-630 RelatedInformation
Publication Year: 2018
Publication Date: 2018-07-17
Language: en
Type: article
Indexed In: ['crossref', 'pubmed']
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Cited By Count: 51
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