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논문 기본 정보

자료유형
학술저널
저자정보
Ho-Ryun Won (Otolaryngology-Head and Neck Surgery Chungnam National University Hospital Daejeon Korea) Chorong Seo (Department of Otolaryngology Ajou University Scho) Hye-Young Lee (Department of Otolaryngology Ajou University Scho) 노진 (아주대학교) Chul-Ho Kim (Department of Otolaryngology Ajou University School of Medicine Suwon Korea) Jeon Yeob Jang (Department of Otolaryngology Ajou University School of Medicine Suwon Korea) Yoo Seob Shin (Department of Otolaryngology Ajou University School of Medicine Suwon Korea)
저널정보
한국조직공학과 재생의학회 조직공학과 재생의학 조직공학과 재생의학 제16권 제6호
발행연도
2019.1
수록면
667 - 674 (8page)

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BACKGROUND: Macrophages have been known to have diverse roles either after tissue damage or during the wound healing process; however, their roles in flap wound healing are poorly understood. In this study, we aimed to evaluate how macrophages contribute to the flap wound regeneration. METHODS: A murine model of a pedicled flap was generated, and the time-course of the wound healing process was determined. Especially, the interface between the flap and the residual tissue was histopathologically evaluated. Using clodronate liposome, a macrophage-depleting agent, the functional role of macrophages in flap wound healing was investigated. Coculture of human keratinocyte cell line HaCaT and monocytic cell line THP-1 was performed to unveil relationship between the two cell types. RESULTS: Macrophage depletion significantly impaired flap wound healing process showing increased necrotic area after clodronate liposome administration. Interestingly, microscopic evaluation revealed that epithelial remodeling between the flap tissue and residual normal tissue did not occurred under the lack of macrophage infiltration. Coculture and scratch wound healing assays indicated that macrophages significantly affected the migration of keratinocytes. CONCLUSION: Macrophages play a critical role in the flap wound regeneration. Especially, epithelial remodeling at the flap margin is dependent on proper macrophage infiltration. These results implicate to support the cellular mechanisms of impaired flap wound healing.

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