Antenatal priming theory about induction of neonatal chronic lung disease: collapse of redox balance.

• Project/Area Number: 23791239
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Embryonic/Neonatal medicine
• Research Institution: Osaka Medical College
• Principal Investigator: HASEGAWA Masashi 大阪医科大学, 医学部, 助教 (80388264)
• Project Period (FY): 2011 – 2012
• Project Status: Completed (Fiscal Year 2012)
• Budget Amount: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000); Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000); Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
• Keywords: 未熟児医学 / 慢性肺疾患 / 上皮間質転換 / 酸化還元状態 / 活性酸素

Research Abstract

I think that neonatal chronic lung disease may have been developed by prenatal changes of the redox state, and tested the assumption in a cell model. Epithelial mesenchymal transition (EMT) is enhanced by exposure of TNFα and TGFβ to L2 cells. Intracellular GSH decreased after addition of TGFβ, and EMT is more enhanced by GSH depletion and TNFα preload. Intracellular hydrogen peroxide increased by TNFα preload and EMT is reduced by the addition of catalase mimic. I think that redox status of cells influence the cellular response to prenatal stress.