| Project/Area Number |
15K21334
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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 |
Pediatrics
Embryonic/Neonatal medicine
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| Research Institution | Saitama Medical University |
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Principal Investigator |
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| Research Collaborator |
NAMBA Fumihiko 埼玉医科大学, 小児科, 講師 (20643323)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 高濃度酸素 / 新生児 / 肺傷害 / BTB and CNC homology 1 / 高濃度酸素性肺傷害 / マウス / 肺胞化 / heme oxygenase / 炎症性サイトカイン / 気管支肺異形成 |
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| Outline of Final Research Achievements |
Bach1 is a transcriptional repressor of HO-1. The effects of Bach1 disruption on hyperoxic lung injury in newborn mice have not been determined. We aimed to investigate the role of Bach1 in the newborns exposed to hyperoxia. Bach1-/- and WT newborn mice were exposed to 21% or 95% oxygen for 4 days. Lung histology was assessed and lung Bach1, HO-1, IL-6, and MCP-1 mRNA levels were evaluated. Lung inflammatory cytokine levels were determined using cytometric bead arrays. After 10 days recovery from neonatal hyperoxia, Bach1-/- mice showed improved lung alveolarization compared with WT. HO-1, IL-6, and MCP-1 mRNA levels and IL-6 and MCP-1 protein levels were significantly increased in the Bach1-/- lungs exposed to neonatal hyperoxia. Bach1-/- newborn mice were well-recovered from hyperoxia-induced lung injury. This effect is likely achieved by the antioxidant/anti-inflammatory activity of HO-1 or by the transient overexpression of proinflammatory cytokines.
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