2016 Fiscal Year Final Research Report
A Novel Strategy for Controlling Chronic Inflammation and Fibrosis: Targeting Sphingolipid Signaling
Project/Area Number |
26460374
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General medical chemistry
|
Research Institution | Ishikawa Prefectural Nursing University |
Principal Investigator |
Takuwa Noriko 石川県立看護大学, 看護学部, 教授 (70150290)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | スフィンゴシン-1-リン酸 / 情報伝達 / 慢性炎症 / 臓器線維化 |
Outline of Final Research Achievements |
Molecular mechanism for organ fibrosis is not understood to date, with useful medicine to be developed. In our bloodstream is a lipid mediator named sphingosine-1-phosphate (S1P), which acts via 5 members of the S1P receptors to play diverse roles. S1P is also involved in pathophysiology of many kinds of diseases and disorders. We previously discovered that too much production of S1P in the heart in transgenic mice, which expressed high levels of S1P synthesizing enzyme, developed heart fibrosis spontaneously with age. In the present study we examined whether and how S1P signaling is involved in development of bleomycin (an anticancer chemotherapeutic that induce lung fibrosis as a side effect)-induced lung fibrosis. We found that one of the S1P receptors mediates aggravation of lung fibrosis, by using knockout mice and the S1P receptor subtype-specific antagonist, which is a promising candidate for treatment of human organ fibrosis.
|
Free Research Field |
病態生理
|