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Contribution of IFNg to thrombotic formation and endothelial damage and clarification of development in chronic thromboembolic pulmonary hypertension

Research Project

Project/Area Number 26893035
Research Category

Grant-in-Aid for Research Activity Start-up

Allocation TypeSingle-year Grants
Research Field Respiratory organ internal medicine
Research InstitutionChiba University

Principal Investigator

Shigeta Ayako  千葉大学, 医学(系)研究科(研究院), 寄付講座教員 (70436369)

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)
KeywordsIFNγ / 慢性血栓塞栓性肺高血圧症 / 肺動脈内皮細胞 / 肺動脈平滑筋細胞
Outline of Final Research Achievements

In this study, It was estimated if IFNγ would relate to development of chronic thromboembolic pulmonary hypertension. We divided patients with CTEPH into 2 group depending on serum IFNγ within measuring range of serum IFNγ or more than it. Patients with IFNγ more than measuring range had significant more peripheral thrombosis. INFγ stimulation induced production of inflammatory cytokines and cell attachment molecules in pulmonary arterial endothelial cels. In terms of endothelial cells derived from removed thrombosis by pulmonary endoarterectomy, RNA expression related to inflammation were much higher even without IFNγ stimulation and induced further with IFNγ stimulation. However interestingly, IFNγ stimulation reduced RNA expression related to coagulation.

Report

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

URL: 

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

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