Is inducion of osteoblasts proliferation useful to treat the osteporosis patients?

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K07950
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: Hoshi University
• Principal Investigator: Takahashi Katsuhiko 星薬科大学, 薬学部, 准教授 (80307066)
• Co-Investigator(Kenkyū-buntansha): 内田 隆史 東北大学, 農学研究科, 教授 (80312239)
• Co-Investigator(Renkei-kenkyūsha): Amano Hitoshi 大阪歯科大学, 歯学部, 准教授 (90212571) ; Takahashi Noriko 星薬科大学, 薬学部, 教授 (50277696)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 骨代謝 / p57Kip2 / Pin1 / 細胞周期 / 骨粗鬆症

Outline of Final Research Achievements

We expected that suppression of p57Kip2 could increase osteoblastic proliferation, resulted in improvement of osteoporosis patients. A cell cycle regulator, p57Kip2-null mice had osteoblasts with high proliferation rates and their osteoclasts maturation were less than the wild-type mice. On the other hand, a cell cycle acceleration prolyl isomerase, Pin1-null mice displayed typical osteoporotic symptoms with many maturated osteoclasts. Then we created p57Kip2/Pin1 double deficient mice, which also showed the phenotypes similar to p57Kip2-null mice. So we thought that p57Kip2 might be under Pin1 in osteoblasts,and the osteoporosis with Pin1 inactivation could be improved by p57Kip2 suppression.

Free Research Field

生化学