The role of S1P3 signaling in the bone metabolism

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09533
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Collagenous pathology/Allergology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: KOHNO Masataka 京都府立医科大学, 医学(系)研究科(研究院), 講師 (60405256)
• Co-Investigator(Kenkyū-buntansha): 川人 豊 京都府立医科大学, 医学(系)研究科(研究院), 准教授 (50336731) ; 中田 博 京都産業大学, 総合生命科学部, 教授 (90113141)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: スフィンゴシン１リン酸 / S1P3受容体 / S1P3-KOマウス / 骨粗しょう症 / 破骨細胞

Outline of Final Research Achievements

The role of S1P3 receptor signaling in bone metabolism is poorly understood. Thus, we examined the mechanisms in the development of osteoporosis which were induced by ovariectomy in murine. pQCT showed that S1P3-/- (KO) mice had significantly lower bone mineral density compared with wild type (WT) in the 28 th day.
Osteoclast precursors obtained from femoral bone marrow were cultured for 7 days in the medium containing M-CSF. The adherent cells were resuspended and seeded on the culture plate coated with an inorganic crystalline calcium phosphate. These cells were cultured in the medium containing M-CSF and RANKL with or without variable concentration of S1P and area of absorption pits were cumulated and compared with each others. There was no significant differences of pit areas between WT and S1P3-KO in physiological concentrations(0, 0.1, 1microM) of S1P. It was suggested that S1P-S1P3 signaling in osteoclast didn't make a significant contribution to its activity.

Free Research Field

リウマチ・膠原病