| Project/Area Number |
16K20361
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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 |
Plastic surgery
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| Research Institution | Nagasaki University |
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Principal Investigator |
TANAKA Katsuya 長崎大学, 医歯薬学総合研究科(医学系), 研究協力員 (70722750)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | miRNA / 炎症 / イメージング / 皮膚創傷治癒 / 好中球 / 感染 / 黄色ブドウ球菌 / microRNA / 瘢痕・ケロイド / イメージング解析 |
|---|
| Outline of Final Research Achievements |
MicroRNAs are small noncoding RNAs that regulate protein translation by binding to complementary target mRNAs. In this study, we generated miR-142 knockout (KO) mice and showed that healing of Staphylococcus aureus-infected skin wounds was significantly delayed in miR-142 KO mice compared with that in wild-type mice. MiR-142 KO neutrophils showed altered phagocytosis as a consequence of chemotactic behavior, including enhanced F-actin assembly, disturbed cell polarity, and increased cell motility. We showed that these changes were linked to cytoskeletal regulation, and that expression of the small GTPases was markedly increased in miR-142－/－ neutrophils. Collectively, our data demonstrate that the miR-142 family is indispensable for protection against S. aureus infection and its clearance at wound sites. MiR-142-3p and miR-142-5p play nonredundant roles in actin cytoskeleton regulation by controlling small GTPase translation in neutrophils at wound sites.
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