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

CaMK4 inhitotion in rheumatoid arthritis for the immunological remission

Research Project

Project/Area Number 26893198
Research Category

Grant-in-Aid for Research Activity Start-up

Allocation TypeSingle-year Grants
Research Field Collagenous pathology/Allergology
Research InstitutionNagasaki University

Principal Investigator

KOGA Tomohiro  長崎大学, 病院(医学系), 助教 (90537284)

Project Period (FY) 2014-08-29 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywords関節リウマチ / CaMK4 / 関節炎誘導マウス
Outline of Final Research Achievements

We investigated the relationship between RA development and the expression of CaMK4 in CD4 T cell and found that the level of Camk4 mRNA was significantly higher in patients with RA.
This data indicated the abnormal CaMK4 expression and function contributes to the pathogenesis of RA. We further examined the relationship between CaMK4 expression and disease activity among RA patients but there was no significant difference.
To determine the protective effect on collagen induced arthritis in mice, we treated with the CaMK4 inhibitor. Importantly, the group treated with CaMK4 inhibitor exhibited the significant improvement of arthritis indicating the possible therapeutic target for RA.

Report

(3 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2014 Annual Research Report
  • Research Products

    (3 results)

All 2016 2014

All Journal Article (1 results) (of which Int'l Joint Research: 1 results,  Peer Reviewed: 1 results,  Open Access: 1 results,  Acknowledgement Compliant: 1 results) Presentation (2 results)

  • [Journal Article] CaMK4 facilitates the recruitment of IL-17-producing cells to target organs through the CCR6/CCL20 axis in Th17-driven inflammatory diseases.2016

    • Author(s)
      Koga T, Otomo K, Mizui M, Yoshida N, Umeda M, Ichinose K, Kawakami A, Tsokos GC
    • Journal Title

      Arthritis Rheumatol.

      Volume: in press Issue: 8 Pages: 1981-1988

    • DOI

      10.1002/art.39665

    • Related Report
      2015 Annual Research Report
    • Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
  • [Presentation] Role of CaMK4 in the pathogenesis of rheumatoid arthritis2016

    • Author(s)
      Tomohiro Koga,Masataka Umeda,Yasuko Hirai,Toru Michitsuji,Toshimasa Shimizu,Shoichi Fukui,Ayako Nishino,Yoshikazu Nakashima,Shin-ya Kawashiri,Naoki Iwamoto,Kunihiro Ichinose,Mami Tamai,Tomoki Origuchi,Hideki Nakamura,Atsushi Kawakami
    • Organizer
      第60回日本リウマチ学会総会
    • Place of Presentation
      パシフィコ横浜(神奈川県横浜市)
    • Year and Date
      2016-04-21
    • Related Report
      2015 Annual Research Report
  • [Presentation] CaMK4 inhibition ameliorates the development of Th17 driven inflammatory diseases by preventing recruitment of IL-17 producing cells to target organs2014

    • Author(s)
      Tomohiro Koga
    • Organizer
      2014年米国リウマチ学会議(ACR 2014)
    • Place of Presentation
      ボストン、米国
    • Year and Date
      2014-11-14 – 2014-11-18
    • Related Report
      2014 Annual Research Report

URL: 

Published: 2014-09-09   Modified: 2017-05-10  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi