Mechanism and expression of CD302 as a new regulator of osteoclast maturation

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K11038
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Functional basic dentistry
• Research Institution: Okayama University
• Principal Investigator: Aoyama Eriko 岡山大学, 医歯薬学総合研究科, 助教 (10432650)
• Co-Investigator(Kenkyū-buntansha): 滝川 正春 岡山大学, 医歯薬学総合研究科, 教授 (20112063) ; 服部 高子 岡山大学, 医歯薬学総合研究科, 助教 (00228488) ; 西田 崇 岡山大学, 医歯薬学総合研究科, 准教授 (30322233) ; 久保田 聡 岡山大学, 医歯薬学総合研究科, 教授 (90221936)
• Co-Investigator(Renkei-kenkyūsha): HOSHIJIMA Mitsuhiro 岡山大学, 医歯薬学総合研究科, 助教 (30736567)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 破骨細胞 / アクチンリング / CD302/DCL-1 / 骨吸収

Outline of Final Research Achievements

CD302/DCL-1 is one of the C-type lectin receptors, but the distribution and the function has been mostly not clarified. We found that CD302 was expressed on osteoclasts induced from murine bone marrow cells. The inhibition of CD302 expression caused fragmentation of actin ring in mature osteoclasts and reduced bone resorption in vitro. Also, CD302 was co-localized with CCN2 which is a positive regulator of osteoclast maturation. Moreover, SHP-2 was identified as a potent candidate as a signal transducer of CD302 signaling. These results showed that CD302 could be a new target protein to regulate osteoclast maturation.

Free Research Field

生化学、 骨代謝学