2011 Fiscal Year Final Research Report
Regulation of inflammatory bone destruction by galectin 3 : Identification of the novel receptor and molecular histological research
| Project/Area Number |
21592332
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
LI Yinji 九州大学, 歯学研究院, 助教 (90457424)
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| Co-Investigator(Kenkyū-buntansha) |
久木田 敏夫 (30153266)
久木田 明子 (30153266)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 口腔解剖学(含組織学・発生学) |
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| Research Abstract |
Galectin 3 is the factor which regulates inflammatory bone destruction and suppresses osteoclastogenesis. As the inhibitory activity of galectin 3 was not attributed to the carbohydrate recognition domain(CRD), N-terminal region was considered to have regulatory roles in the regulation of osteoclastogenesis. N-terminal region of galectin-3 was recloned and recombinant protein was obtained, however, we have failed in obtaining active recombinant polypeptides bearing inhibitory activity on osteoclastogenesis. We then examined other types of galectin. Galectin 9 is the tandem type of galectin with two CRDs connected by a linker polypeptide. Galectin 1 is the prototype galectin composed of only two CRD. Although galectin 1 did not affect osteoclastogenesis, galectin 9 markedly inhibited osteoclastogenesis in a dose-dependent manner. The inhibition of osteoclastogenesis by galectin 9 was partly canceled by the addition of lactose. It was strongly suggested the presence of CRD-dependent mechanism as well as CRD-independent mechanism. We further examined if the galectin 9 receptor is expressed in osteoclast precursors and found that some receptor molecules regulating apoptosis are expressed in osteoclast precursors. This research would provide important tool and strategy for controlling inflammatory bone destruction.
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Research Products
(14 results)
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[Journal Article] The Transcription Factor FBI-1/OCZF/LRF Is Expressed in Osteoclasts and Regulates RANKL-Induced Osteoclast Formation In Vitro and In Vivo2011
Author(s)
Kukita A., Kukita T., , Nagata K., Teramachi J., Li Y-J., Yoshida H., Miyamoto H., Gay S., Pessler F., Shobuike T.
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Journal Title
Arth Rheumatism
Volume: 63(9)
Pages: 2744-2754
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