書誌事項
- タイトル別名
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- Gene Therapy for Tracheal Stenosis Using Sendai Virus Vector
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Acquired tracheal stenosis remains a challenging problem for otolaryngologists. The objective of this study was to determine whether the Sendai virus(SeV)-mediated c-myc suppressor, a far upstream element(FUSE)-binding protein(FBP)-interacting repressor(FIR), modulates wound healing of the airway mucosa, and whether it prevents tracheal stenosis in an animal model of induced mucosal injury. First, a novel animal model for LTS was established. Next, we successfully demonstrated SeV-mediated transgene expression in the injured mucosa of the LTS model. Finally, a fusion gene-deleted, non-transmissible SeV vector encoding FIR(FIR-SeV/ΔF)was prepared. FIR-SeV/ΔF was administered to the rats with scraped airway mucosae through the tracheostoma. Untreated animals showed hyperplasia of the airway epithelium and a thickened submucosal layer with extensive fibrosis, angiogenesis, and collagen deposition causing lumen stenosis. In contrast, the administration of FIR-SeV/ΔF decreased the degree of tracheal stenosis and improved the survival rate. Immunohistochemical staining showed that c-Myc expression was downregulated in the tracheal basal cells of the FIRSeV/ΔF-treated animals, suggesting that c-myc was suppressed by FIR-SeV/ΔF in the regenerating airway epithelium of the injured tracheal mucosa. The airway-targeted gene therapy of the c-myc suppressor FIR, using a recombinant SeV vector, prevented tracheal stenosis in a rat model of airway mucosal injury.
収録刊行物
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- 喉頭
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喉頭 27 (2), 51-58, 2015
日本喉頭科学会
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詳細情報 詳細情報について
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- CRID
- 1390001204352145536
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- NII論文ID
- 130005164818
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- ISSN
- 21854696
- 09156127
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可