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Notch1 信号通路促进缺氧诱导的角质形成细胞迁移中整合素 β1 的高表达。

Notch1 Signaling Contributes to Hypoxia-induced High Expression of Integrin β1 in Keratinocyte Migration.

机构信息

Institute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, The Third Military Medical University, Chongqing, China.

出版信息

Sci Rep. 2017 Mar 7;7:43926. doi: 10.1038/srep43926.

Abstract

Oxygen tension is an important micro-environmental factor that affects epidermal development and function. After injury, high oxygen consumption and vascular injury result in partial hypoxia. However, whether hypoxia benefits or hurts wound healing remains controversial. In this study, a tissue oxygen tension monitor was used to detect the spatial and temporal distribution of oxygen in burn wounds. In vitro, we demonstrate that hypoxia promoted the expression of integrin β1 and the migration of keratinocytes. Furthermore, hypoxia-induced migration was slowed by Notch1 ligands and a siRNA against ITGB1 (integrin β1). Our findings suggest that integrin β1 may be an oxygen-sensitive molecule that promotes keratinocyte migration during wound healing and that Notch1 signaling is involved in this process.

摘要

氧张力是影响表皮发育和功能的重要微环境因素。损伤后,高耗氧量和血管损伤导致局部缺氧。然而,缺氧对伤口愈合是有益还是有害仍存在争议。在这项研究中,我们使用组织氧张力监测仪检测烧伤创面的氧时空分布。在体外,我们证明缺氧促进整合素β1的表达和角质形成细胞的迁移。此外,Notch1 配体和针对 ITGB1(整合素β1)的 siRNA 减缓了缺氧诱导的迁移。我们的研究结果表明,整合素β1可能是一种氧敏感分子,它在伤口愈合过程中促进角质形成细胞迁移,而 Notch1 信号通路参与了这一过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac62/5339698/908511aa9eba/srep43926-f5.jpg

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