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Tenascin-C promotes the repair of cartilage defects in mice.

Authors
  • Unno, Hironori1
  • Hasegawa, Masahiro2
  • Suzuki, Yoshiaki1
  • Iino, Takahiro1
  • Imanaka-Yoshida, Kyoko3
  • Yoshida, Toshimichi3
  • Sudo, Akihiro1
  • 1 Department of Orthopaedic Surgery, Mie University Graduate School of Medicine, Mie, Japan. , (Japan)
  • 2 Department of Orthopaedic Surgery, Mie University Graduate School of Medicine, Mie, Japan. Electronic address: masah[email protected] , (Japan)
  • 3 Department of Pathology & Matrix Biology, Mie University Graduate School of Medicine, Mie, Japan. , (Japan)
Type
Published Article
Journal
Journal of Orthopaedic Science
Publisher
Elsevier
Publication Date
Mar 01, 2020
Volume
25
Issue
2
Pages
324–330
Identifiers
DOI: 10.1016/j.jos.2019.03.013
PMID: 30975540
Source
Medline
Language
English
License
Unknown

Abstract

The effects of tenascin-C (TNC) on cartilage repair were examined in cartilage defect model mice. An in vitro study was also performed to determine the mechanism of cartilage repair with TNC. Full-thickness osteochondral defects were filled with TNC (group A: 100 μg/ml, group B: 10 μg/ml, group C: empty). Mice were sacrificed at 1, 2, 3, and 6 weeks postoperatively. Cartilage repair was histologically evaluated using the modified WAKITANI score. Chondrocytes were isolated and cultured, and they were treated with TNC. The expressions of various mRNAs including TNC, inflammatory cytokines, and anabolic and catabolic factors for cartilage were compared by real-time polymerase chain reaction. The defects in group A were covered with hyaline-like cartilage after 3 weeks. Average modified WAKITANI scores were significantly better in group A than in groups B and C at 3 and 6 weeks. TNC upregulated the expressions of endogenous TNC, inflammatory cytokines, and anabolic and catabolic factors for cartilage. TNC downregulated the expression of a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) 5. Intra-articular injection of full-length TNC repaired cartilage in murine models of full-thickness osteochondral defects. TNC upregulated the expression of ADAMTS4, but downregulated the expression of ADAMTS5 that contributed to cartilage degradation. Copyright © 2019 The Japanese Orthopaedic Association. Published by Elsevier B.V. All rights reserved.

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