Efficacy of PAR-2 antagonists in lung fibrosis
| Project/Area Number |
23591159
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Fukushima Medical University (2013-2014)
Saitama Medical University (2011-2012) |
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Principal Investigator |
SUZUKI TOMOKO 福島県立医科大学, 公私立大学の部局等, 准教授 (10400342)
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 肺線維症急性増悪 / 国際情報交流 |
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| Outline of Final Research Achievements |
Pathogenetic mechanisms of idiopathic interstitial pneumonias (IIPs) remain unclear. Epithelial-to-mesenchymal transition (EMT) may play a key in the pathogenesis of fibrosis. Transforming growth factor (TGF)-beta is known to induce the transformation of fibroblasts to myofibroblasts and EMT of epithelium. Protease activated receptor (PAR)-2 has been recognized as a key molecule regulating inflammation and fibrosis. We hypothesized that PAR-2 activation induces TGF-beta and EMT.
Functional PAR-2 was expressed on lung epithelium. PAR-2 activation by trypsin or PAR-2AP induced TGF-beta. PAR-2 activation led to cleavage of E-cadherin and induction of vimentin expression. These phenomena were blocked by PAR-2 inhibiting peptide. PAR-2 activation induces TGF-beta and EMT of lung epithelium, processes that may contribute to lung fibrosis. PAR-2 may be a key molecule driving lung fibrosis and thus represent a novel therapeutic target.
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Report
(5 results)
Research Products
(3 results)
