Development of transplanted lung function-preserving method using a mouse model focusing on the anti-inflammatory related molecule Spred2

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K09306
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 55040:Respiratory surgery-related
• Research Institution: Shimane University (2021); Okayama University (2019-2020)
• Principal Investigator: Yamane Masaomi 島根大学, 学術研究院医学・看護学系, 教授 (20432643)
• Co-Investigator(Kenkyū-buntansha): 豊岡 伸一 岡山大学, 医歯薬学総合研究科, 教授 (30397880) ; 松川 昭博 岡山大学, 医歯薬学総合研究科, 教授 (90264283)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 急性肺障害 / 肺移植 / 移植免疫 / 急性拒絶

Outline of Final Research Achievements

A lung injury experiment using a thoracotomy and clamp model was also performed using Spred2 knockout mice and transgenic mice that are Spred2 gene overexpressing mice. Histological images by RT-PCR and H-E staining and arterial gas analysis were performed and evaluated as preliminary experiments, but no difference was observed. Furthermore, the expression level was confirmed by Western blotting using an anti-mouse SPRED2 antibody, but no difference was observed in the preliminary experiment.
Overexpression of Spred2 at protein and mRNA levels could not be confirmed in Spred2 transgenic mice and conditional knockout mice specifically deficient in bone marrow-derived cells, compared with wild-type in experiments using a hilar clamp model. No significant difference was found in ischemia-reperfusion injury.

Free Research Field

肺移植、急性肺障害

Academic Significance and Societal Importance of the Research Achievements

これまでSpred2と移植後急性肺障害との関係を明らかにすべく報告してきた。今回はコンディショナルノックアウトマウスを開発し急性肺障害、さらには急性拒絶との関連を試みた。しかしながらトランスジェニックマウス、コンディショナルノックアウトマウスによる実験系では有意な差を見出すことはできず、急性肺障害とMAPキナーゼ系との関与についてさらなる研究が必要である。