The inhibitory role of incretin mimetics against lung injury-induced by Toll-like receptor-mediated signaling.
| Project/Area Number |
23790924
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 肺線維症 / 肺傷害 / インクレチン |
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| Research Abstract |
Glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide(GIP) are known incretin hormones. To elucidate the potential role of incretins in prevention of lung injury, we analyzed the expression of incretin receptors and effect of exendin-4, a GLP-1 receptor agonist. Although neither expression of incretin receptors nor effect of exendin-4 was demonstrated in cell culturing models, type II pneumocytes in lung tissue expressed GLP-1 receptor. GLP-1 receptor expression in type II pneumocyte was especially increased in idiopathic pulmonary fibrosis (IPF), suggesting the potential involvement of incretin in IPF pathogenesis.
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Report
(3 results)
Research Products
(6 results)
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[Journal Article] Insufficient autophagy promotes bronchial epithelial cell senescence in chronic obstructive pulmonary disease.2012
Author(s)
Fujii S, Hara H, Araya J, Takasaka N, Kojima J, Ito S, Minagawa S, Yumino Y, Ishikawa T, Numata T,Kawaishi M, Hirano J, Odaka M, Morikawa T, Nishimura SL, Nakayama K, Kuwano K.
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Journal Title
Oncoimmunology
Volume: 1(5)
Pages: 630-641
Related Report
Peer Reviewed
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