| Project/Area Number |
17K18005
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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 |
Embryonic/Neonatal medicine
Pediatrics
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| Research Institution | Nagoya City University |
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Principal Investigator |
Kato Shin 名古屋市立大学, 医薬学総合研究院(医学), 助教 (90551250)
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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 |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 慢性肺疾患 / 早産児 / 肺胞形成 / 前駆タンパク質転換酵素 / myofibroblast / furin / マウス / 酸素投与 / 組織染色 / 細胞染色 / western blotting / 前駆体蛋白変換酵素 / 炎症 / 未熟児慢性肺疾患 / 未熟児医学 / 小児呼吸器学 / 小児科学 |
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| Outline of Final Research Achievements |
We hypothesized that furin, also known as an enzyme that cleaves proproteins of factors involved in alveologenesis, may play a key role in the pathogenesis of chronic lung disease in preterm infants. Here we examined its role using a chronic lung disease model in neonatal mice exposed to 85% oxygen. We showed that furin is expressed in myofibroblasts in mouse lungs, and that the expression of furin and its target proteins is decreased in the mouse model, resulting in worsened alveoli formation. Next, we showed that administration of a furin inhibitor successfully reproduced the pathology. Finally, we showed that treatment with furin improved alveoli formation in a hyperoxia-exposed mouse model.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究で我々は、早産児に特有の慢性肺疾患の病因として、新規にfurinが重要な役割を果たしていることを世界で初めて明らかにした。標準治療では改善が困難な重症の慢性肺疾患において、新規治療戦略の選択肢となりうる。毎年およそ1200人前後と推計される罹患児の長期予後の改善から社会参画の促進や医療費の抑制につながることも期待できるなど、社会的意義が非常に大きい。
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