The role of platelets in the mechanism of pathogenesis of bronchial asthma
| Project/Area Number |
17K11976
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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 |
Orthodontics/Pediatric dentistry
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| Research Institution | Tsurumi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
脇田 亮 東京医科歯科大学, 大学院医歯学総合研究科, 准教授 (60376712)
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| Project Period (FY) |
2017-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 気管支喘息 / 気管支平滑筋 / 細胞増殖 / 血小板 / 喘息 / ぜんそく |
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| Outline of Final Research Achievements |
To elucidate the mechanism of platelet-derived growth factor (PDGF)-induced airway smooth muscle cells proliferation in bronchial asthma, human airway smooth muscle cells stably transfected with the Neurokinin-1 receptor were pretreated with G protein βγ signaling inhibitor (Gallein). PDGF-induced cell proliferation was inhibited by Gallein, and the inhibitory effect was stronger than that of SM-SubP, an NK1 receptor agonist we reported previously. In addition, our experiment of LAM cells showed that the dysregulation of PTEN-mediated inhibition of cell proliferation may be one of the mechanisms of abnormal cell proliferation in LAM cells.
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| Academic Significance and Societal Importance of the Research Achievements |
気管支喘息は気道過敏性の亢進，気道狭窄を特徴とする慢性閉塞性の肺疾患である．G蛋白βγシグナリング阻害薬（Gallein）はPI3KおよびRac1を介するシグナリングを抑制する．本研究により，G蛋白βγサブユニットが，NK1受容体を介するPDGFの気管支平滑筋細胞増殖に関与することが示唆された．気管支平滑筋の細胞増殖に関わる分子シグナル伝達経路は，喘息由来の気管支狭窄に対して潜在的治療標的になる可能性が考えられ，この分野の新しい治療法が確立できれば，学術的および社会的にも意義の高いものになる．
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Report
(6 results)
Research Products
(9 results)
