Analysis of the function of Sp7 in osteoclastogenesis using osteoblast-specific Sp7 knockout mice

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K18946
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 57010:Oral biological science-related
• Research Institution: Nagasaki University
• Principal Investigator: KOMORI Hisato 長崎大学, 医歯薬学総合研究科(歯学系), 特任研究員 (80770411)
• Project Period (FY): 2019-04-01 – 2021-03-31
• Keywords: Sp7 / 破骨細胞 / 骨吸収

Outline of Final Research Achievements

To clarify the function of Sp7 after the differentiation into osteoblasts, we generated 2.3 kb Col1a1 promoter-GFP-Cre transgenic mice. Using these mice, we further generated osteoblast-specific Sp7-deficient mice. The trabecular bone was increased and cortical bones was reduced in micro-CT analysis, and the cortical bone was porous and many TRAP-positive osteoclasts were observed in the cortical bone in histological analysis. TUNEL-positive apoptotic osteocytes were increased in the cortical bone. Porous cortical bone was considered to be caused by the increase of osteocyte apoptosis, which enhances osteoclastogenesis.

Free Research Field

骨代謝学

Academic Significance and Societal Importance of the Research Achievements

Sp7は前骨芽細胞から骨芽細胞への分化に必須な転写因子である。しかし、骨芽細胞分化後の機能は、まだ明確になっていない。それは、これまで使われてきた骨芽細胞特異的に発現する2.3 kb Col1a1 Creトランスジェニックマウスの発現レベルが低く、明確な表現型を得にくかったことが原因と考えられる。我々は、新たに2.3 kb Col1a1 GFP-Creトランスジェニックマウスを作製し、Sp7を骨芽細胞特異的に欠失させ、骨細胞の生存におけるその重要性を明らかにした。