Regulation of osteoclastogenesis through Tim-3

Possible involvement of the Tim-3/galectin-9 system in the modulation of inflammatory bone destruction

Kanako Moriyama, Akiko Kukita, Yin Ji Li, Norihisa Uehara, Jing Qi Zhang, Ichiro Takahashi, Toshio Kukita

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Galectins are a unique family of lectins bearing one or two carbohydrate recognition domains (CRDs) that have the ability to bind molecules with β-galactoside-containing carbohydrates. It has been shown that galectins regulate not only cell growth and differentiation but also immune responses, as well as inflammation. Galectin-9, a tandem repeat type of galectin, was originally identified as a chemotactic factor for eosinophils, and is also involved in the regulatory process of inflammation. Here, we examined the involvement of galectin-9 and its receptor, T-cell immunoglobulin- and mucin-domain-containing molecule 3 (Tim-3), in the control of osteoclastogenesis and inflammatory bone destruction. Expression of Tim-3 was detected in osteoclasts and its mononuclear precursors in vivo and in vitro. Galectin-9 markedly inhibited osteoclastogenesis as evaluated in osteoclast precursor cell line RAW-D cells and primary bone marrow cells of mice and rats. The inhibitory effects of galectin-9 on osteoclastogenesis was negated by the addition of β-lactose, an antagonist for galectin binding, suggesting that the inhibitory effect of galectin-9 was mediated through CRD. When galectin-9 was injected into rats with adjuvant-induced arthritis, marked suppression of bone destruction was observed. Inflammatory bone destruction could be efficiently ameliorated by controlling the Tim-3/galectin-9 system in rheumatoid arthritis.

Original languageEnglish
Pages (from-to)1200-1211
Number of pages12
JournalLaboratory Investigation
Volume94
Issue number11
DOIs
Publication statusPublished - Jan 1 2014

Fingerprint

Galectins
Galectin 3
Osteogenesis
Bone and Bones
Carbohydrates
Osteoclasts
Eosinophil Chemotactic Factors
Inflammation
Galactosides
Tandem Repeat Sequences
Experimental Arthritis
Somatostatin-Secreting Cells
Mucins
Lactose
T-Cell Antigen Receptor
Lectins
Bone Marrow Cells
Cell Differentiation
Rheumatoid Arthritis

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology

Cite this

Regulation of osteoclastogenesis through Tim-3 : Possible involvement of the Tim-3/galectin-9 system in the modulation of inflammatory bone destruction. / Moriyama, Kanako; Kukita, Akiko; Li, Yin Ji; Uehara, Norihisa; Zhang, Jing Qi; Takahashi, Ichiro; Kukita, Toshio.

In: Laboratory Investigation, Vol. 94, No. 11, 01.01.2014, p. 1200-1211.

Research output: Contribution to journalArticle

@article{a9c824c63c0d4094a4540bee4866b787,
title = "Regulation of osteoclastogenesis through Tim-3: Possible involvement of the Tim-3/galectin-9 system in the modulation of inflammatory bone destruction",
abstract = "Galectins are a unique family of lectins bearing one or two carbohydrate recognition domains (CRDs) that have the ability to bind molecules with β-galactoside-containing carbohydrates. It has been shown that galectins regulate not only cell growth and differentiation but also immune responses, as well as inflammation. Galectin-9, a tandem repeat type of galectin, was originally identified as a chemotactic factor for eosinophils, and is also involved in the regulatory process of inflammation. Here, we examined the involvement of galectin-9 and its receptor, T-cell immunoglobulin- and mucin-domain-containing molecule 3 (Tim-3), in the control of osteoclastogenesis and inflammatory bone destruction. Expression of Tim-3 was detected in osteoclasts and its mononuclear precursors in vivo and in vitro. Galectin-9 markedly inhibited osteoclastogenesis as evaluated in osteoclast precursor cell line RAW-D cells and primary bone marrow cells of mice and rats. The inhibitory effects of galectin-9 on osteoclastogenesis was negated by the addition of β-lactose, an antagonist for galectin binding, suggesting that the inhibitory effect of galectin-9 was mediated through CRD. When galectin-9 was injected into rats with adjuvant-induced arthritis, marked suppression of bone destruction was observed. Inflammatory bone destruction could be efficiently ameliorated by controlling the Tim-3/galectin-9 system in rheumatoid arthritis.",
author = "Kanako Moriyama and Akiko Kukita and Li, {Yin Ji} and Norihisa Uehara and Zhang, {Jing Qi} and Ichiro Takahashi and Toshio Kukita",
year = "2014",
month = "1",
day = "1",
doi = "10.1038/labinvest.2014.107",
language = "English",
volume = "94",
pages = "1200--1211",
journal = "Laboratory Investigation",
issn = "0023-6837",
publisher = "Nature Publishing Group",
number = "11",

}

TY - JOUR

T1 - Regulation of osteoclastogenesis through Tim-3

T2 - Possible involvement of the Tim-3/galectin-9 system in the modulation of inflammatory bone destruction

AU - Moriyama, Kanako

AU - Kukita, Akiko

AU - Li, Yin Ji

AU - Uehara, Norihisa

AU - Zhang, Jing Qi

AU - Takahashi, Ichiro

AU - Kukita, Toshio

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Galectins are a unique family of lectins bearing one or two carbohydrate recognition domains (CRDs) that have the ability to bind molecules with β-galactoside-containing carbohydrates. It has been shown that galectins regulate not only cell growth and differentiation but also immune responses, as well as inflammation. Galectin-9, a tandem repeat type of galectin, was originally identified as a chemotactic factor for eosinophils, and is also involved in the regulatory process of inflammation. Here, we examined the involvement of galectin-9 and its receptor, T-cell immunoglobulin- and mucin-domain-containing molecule 3 (Tim-3), in the control of osteoclastogenesis and inflammatory bone destruction. Expression of Tim-3 was detected in osteoclasts and its mononuclear precursors in vivo and in vitro. Galectin-9 markedly inhibited osteoclastogenesis as evaluated in osteoclast precursor cell line RAW-D cells and primary bone marrow cells of mice and rats. The inhibitory effects of galectin-9 on osteoclastogenesis was negated by the addition of β-lactose, an antagonist for galectin binding, suggesting that the inhibitory effect of galectin-9 was mediated through CRD. When galectin-9 was injected into rats with adjuvant-induced arthritis, marked suppression of bone destruction was observed. Inflammatory bone destruction could be efficiently ameliorated by controlling the Tim-3/galectin-9 system in rheumatoid arthritis.

AB - Galectins are a unique family of lectins bearing one or two carbohydrate recognition domains (CRDs) that have the ability to bind molecules with β-galactoside-containing carbohydrates. It has been shown that galectins regulate not only cell growth and differentiation but also immune responses, as well as inflammation. Galectin-9, a tandem repeat type of galectin, was originally identified as a chemotactic factor for eosinophils, and is also involved in the regulatory process of inflammation. Here, we examined the involvement of galectin-9 and its receptor, T-cell immunoglobulin- and mucin-domain-containing molecule 3 (Tim-3), in the control of osteoclastogenesis and inflammatory bone destruction. Expression of Tim-3 was detected in osteoclasts and its mononuclear precursors in vivo and in vitro. Galectin-9 markedly inhibited osteoclastogenesis as evaluated in osteoclast precursor cell line RAW-D cells and primary bone marrow cells of mice and rats. The inhibitory effects of galectin-9 on osteoclastogenesis was negated by the addition of β-lactose, an antagonist for galectin binding, suggesting that the inhibitory effect of galectin-9 was mediated through CRD. When galectin-9 was injected into rats with adjuvant-induced arthritis, marked suppression of bone destruction was observed. Inflammatory bone destruction could be efficiently ameliorated by controlling the Tim-3/galectin-9 system in rheumatoid arthritis.

UR - http://www.scopus.com/inward/record.url?scp=84908473593&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84908473593&partnerID=8YFLogxK

U2 - 10.1038/labinvest.2014.107

DO - 10.1038/labinvest.2014.107

M3 - Article

VL - 94

SP - 1200

EP - 1211

JO - Laboratory Investigation

JF - Laboratory Investigation

SN - 0023-6837

IS - 11

ER -