The impact of ER stress on resolution of inflammation and tissue repair in lung
| Project/Area Number |
24591169
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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 | Nagasaki University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 小胞体ストレス / 慢性肺疾患 / efferocytosis / 肺気腫 / 炎症終息 / 組織修復 / 肺胞マクロファージ / 肺線維症 / 急性肺障害 |
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| Outline of Final Research Achievements |
Endoplasmic Reticulum (ER) stress plays crucial roles in pathogenesis of chronic disease such as atherosclerosis and diabetes. ER stress is induced by over production of protein or accumulation of abnormal protein in cell. I focused on the contribution of ER stress to pathogenesis of chronic lung disease. First we tested the effect of ER stress on alveolar epithelial cells, and proved that it induced hyporesponsiveness to inflammatory stimulation. Then we proved that ER stress may decrease apoptotic cell clearance by alveolar macrophages , that is important in resolution of inflammation, through RhoA activation. Next we used streptozotocin induced hyperglycemic mice to see the effect of ER stress on resolution of inflammation and tissue repair in lung. During lung inflammation by LPS, hyperglycemic mice showed lower production of hepatocyte growth factor in lung but apoptotic cell clearance. We will continue to try to clarify the mechanisms.
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Report
(5 results)
Research Products
(5 results)
