The role of c-Kit in mice model of heterotopic tracheal transplantation

2014 Fiscal Year Final Research Report

• Project/Area Number: 25860639
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Respiratory organ internal medicine
• Research Institution: Kanazawa University
• Principal Investigator: WASEDA Yuko 金沢大学, 医学系, 協力研究員 (80536037)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 病態機序解明

Outline of Final Research Achievements

Tracheal allografts developed epithelial injury and complete luminal occlusion by day 28, whereas isografts showed intact epithelium without relation of c-Kit. Notably, the administration of imatinib, from day 0 of transplantation, to mice recipients of allografts significantly reduced the tracheal luminal occlusion. In addition, in tracheal allografts, the number of fibrocytes increased significantly between days 3 and 7 of transplantation as compared with isografts, and this recipient-derived fibrocyte infiltration was inhibited by imatinib. Analysis of fibrocyte populations in bone marrow and peripheral blood revealed the same trend, with significant lower number of fibrocytes in the allograft recipients treated with imatinib. Furthermore, in vitro studies showed that imatinib inhibited the differentiation of cultured blood derived monocytes into fibrocytes.

Free Research Field

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