• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to project page

2020 Fiscal Year Final Research Report

Analysis of the transcription factor Nfatc1 isoform in osteoclast differentiation

Research Project

  • PDF
Project/Area Number 18K09118
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 56020:Orthopedics-related
Research InstitutionJichi Medical University (2019-2020)
Saitama Medical University (2018)

Principal Investigator

Sato Kojiro  自治医科大学, 医学部, 教授 (10372434)

Project Period (FY) 2018-04-01 – 2021-03-31
Keywords破骨細胞
Outline of Final Research Achievements

It is known that the expression level of a transcription factor Nfatc1 increases drastically in the process of osteoclast differentiation. At least three isoforms are expressed in osteoclasts, among which the shortest isoform increases in osteoclastogenesis. We have made this short isoform-specific knockout (KO) mice using CRISPR/Cas9 system. Homo KO mice are embryonic lethal, and TRAP-positive multi-nucleated cells do not differentiate from hematopoietic stem cells derived from KO fetuses, in contrast to those cells from wild type fetuses.

Free Research Field

臨床免疫学

Academic Significance and Societal Importance of the Research Achievements

この解析から、Nfatc1のbasalの発現だけではマウスは胎性致死に陥ることが判明した。肝臓における造血が不十分であることが一因であると思われる。また、より原始的な造血幹細胞から、単球系細胞は分化するものの破骨細胞は分化しないことから、Nfatc1のshort isoformの発現誘導が破骨細胞分化に必須であることが示された。今後このisoformの転写標的を同定する必要がある。本研究は破骨細胞や造血幹細胞の制御において有用な知見をもたらしつつある。

URL: 

Published: 2022-01-27  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi