Journal
BONE
Volume 44, Issue 5, Pages 849-857Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bone.2009.01.365
Keywords
Galectin-9; Human mesenchymal stem cell; Chondrogenesis; TGF beta 3; Cartilage repair
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Funding
- Japanese Ministry of Education, Culture, Sports, Science, and Technology
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Galectin-9 (Gal-9), a beta-galactoside binding lectin, plays a crucial role in innate and adaptive immunity. in the rat collagen-induced arthritis model, administration of Gal-9 induced repair of existing cartilage injury even when joints were already swollen with cartilage destruction. We thus attempted to explore the role of Gal-9 in chondrocyte differentiation utilizing human mesenchymal stem cell (MSC) pellet Cultures. During chondrogenesis induced by transforming growth factor beta 3 (TGF beta 3), MSCs strongly expressed endogenous Gal-9. Expression of Gal-9 peaked on day 14 and the neutralization of endogenous Gal-9 resulted in the reduced chondrogenesis, indicating possible involvement of Gal-9 in TGF beta-mediated chondrogenesis. In pellets, addition of Gal-9 significantly enhanced TGF beta 3-induced chondrogenesis. as evidenced by increasing proteoglycan content, but not cell proliferation. In the absence of Gal-9, collagen expression by MSCs switched from type I to type II on 28 days after stimulation with TGR beta 3. When MSCs were co-stimulated with Gal-9, the class switch occurred on day 21. In addition, Gal-9 synergistically enhanced TGF beta 3-induced phosphorylation of Smad2, though Gal-9 did not itself induce detectable Smad2 phosphorylation. These results Suggest that Gal-9 has a beneficial effect on cartilage repair in injured joints by induction of differentiation of MSCs into chondrocytes. (C) 2009 Elsevier Inc. All rights reserved.
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