Abstract
Galectin-9 (Gal-9), a β-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 β3 (TGFβ3), 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 TGFβ-mediated chondrogenesis. In pellets, addition of Gal-9 significantly enhanced TGFβ3-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 TGFβ3. When MSCs were co-stimulated with Gal-9, the class switch occurred on day 21. In addition, Gal-9 synergistically enhanced TGFβ3-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.
| Original language | English |
|---|---|
| Pages (from-to) | 849-857 |
| Number of pages | 9 |
| Journal | Bone |
| Volume | 44 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - May 2009 |
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Keywords
- Cartilage repair
- Chondrogenesis
- Galectin-9
- Human mesenchymal stem cell
- TGFβ3
ASJC Scopus subject areas
- Physiology
- Endocrinology, Diabetes and Metabolism
- Histology
Cite this
Galectin-9 accelerates transforming growth factor β3-induced differentiation of human mesenchymal stem cells to chondrocytes. / Arikawa, Tomohiro; Matsukawa, Akihiro; Watanabe, Kota; Sakata, Ken mei; Seki, Masako; Nagayama, Megumi; Takeshita, Keisuke; Ito, Kanako; Niki, Toshiro; Oomizu, Souichi; Shinonaga, Rika; Saita, Naoki; Hirashima, Mitsuomi.
In: Bone, Vol. 44, No. 5, 05.2009, p. 849-857.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Galectin-9 accelerates transforming growth factor β3-induced differentiation of human mesenchymal stem cells to chondrocytes
AU - Arikawa, Tomohiro
AU - Matsukawa, Akihiro
AU - Watanabe, Kota
AU - Sakata, Ken mei
AU - Seki, Masako
AU - Nagayama, Megumi
AU - Takeshita, Keisuke
AU - Ito, Kanako
AU - Niki, Toshiro
AU - Oomizu, Souichi
AU - Shinonaga, Rika
AU - Saita, Naoki
AU - Hirashima, Mitsuomi
PY - 2009/5
Y1 - 2009/5
N2 - Galectin-9 (Gal-9), a β-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 β3 (TGFβ3), 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 TGFβ-mediated chondrogenesis. In pellets, addition of Gal-9 significantly enhanced TGFβ3-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 TGFβ3. When MSCs were co-stimulated with Gal-9, the class switch occurred on day 21. In addition, Gal-9 synergistically enhanced TGFβ3-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.
AB - Galectin-9 (Gal-9), a β-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 β3 (TGFβ3), 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 TGFβ-mediated chondrogenesis. In pellets, addition of Gal-9 significantly enhanced TGFβ3-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 TGFβ3. When MSCs were co-stimulated with Gal-9, the class switch occurred on day 21. In addition, Gal-9 synergistically enhanced TGFβ3-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.
KW - Cartilage repair
KW - Chondrogenesis
KW - Galectin-9
KW - Human mesenchymal stem cell
KW - TGFβ3
UR - http://www.scopus.com/inward/record.url?scp=63449120076&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=63449120076&partnerID=8YFLogxK
U2 - 10.1016/j.bone.2009.01.365
DO - 10.1016/j.bone.2009.01.365
M3 - Article
C2 - 19442617
AN - SCOPUS:63449120076
VL - 44
SP - 849
EP - 857
JO - Bone
JF - Bone
SN - 8756-3282
IS - 5
ER -