The role of PKR on the differentiation of osteoblasts and formation of osteoclasts

2015 Fiscal Year Final Research Report

• Project/Area Number: 25462859
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Morphological basic dentistry
• Research Institution: The University of Tokushima
• Principal Investigator: HANEJI Tatsuji 徳島大学, 大学院医歯薬学研究部, 教授 (50156379)
• Co-Investigator(Kenkyū-buntansha): MORIMOTO Hiroyuki 産業医科大学, 医学部, 教授 (30335806) ; TERAMACHI Jyumpei 徳島大学, 大学院医歯薬研究部, 助教 (20515986)
• Co-Investigator(Renkei-kenkyūsha): OKAMURA Hirohiko 徳島大学, 大学院医歯薬研究部, 准教授 (20380024)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 骨芽細胞 / 破骨細胞 / 骨形成 / 骨吸収 / 人工的歯周炎 / PKR / LPS

Outline of Final Research Achievements

We investigated the roles of PKR in osteoclast formation and bone resorption in vitro and in vivo. LPS induced high levels of PKR in osteoclast precursor　cells. The LPS-induced osteoclast differentiation was markedly suppressed in　the cells pre-treated with PKR inhibitor, C16 and in the cells in which gene silencing of PKR were done. Inhibition of PKR activity in the cells was suppressed the expression of osteoclast differentiation markers including c-fos and NFATc. Bone resorption activity of the LPS-induced osteoclasts was also suppressed by the C16 treatment. Inhibition of PKR activity suppressed the LPS-induced activation of NF-κB and MAPK in osteoclasts. Treatment of C16 effectively prevented the LPS-induced destruction of alveolar bone in the artificial periodontitis in rat. Thus, the present results suggest that PKR plays a pivotal role in the LPS-induced bone loss in periodontitis and PKR inhibition may become an important therapeutic target for periodontitis.

Free Research Field

細胞生物学，組織学