低氧条件下bnip3对表皮细胞迁移的影响及其机制研究外科学烧伤专业论文.docxVIP

第三军医大学硕士学位论文CCK 第三军医大学硕士学位论文 CCK Cell Counting Kit 细胞计数试剂盒 0D Optical density 分光光度值 Min Minute 分钟 d Day 天 h Hour 小时 Gram 克 ANOVA Analysis of variance 方差分析 FAK Focal adhesion kinase 黏着斑激酶 MMP Matrix metalloproteinase 基质金属蛋白酶 Cy3 Cyanine 3 青色素3 siRNA Small interfering RNA 小干扰RNA FITC Fluorescein isothiocyanate 异硫氰酸荧光素 HRE HIF-1 response elements HIF．1反应元件 2 万方数据 第三军医大学硕士学位论文Effects 第三军医大学硕士学位论文 Effects of BNIP3 on keratinocyte migration under ttypoxla and itS Oosslble mecIIanisms Abstract Background Wound healing is a well ordered process that requires the orchestration of a variety of tissues and cells．Re—epithelialization is a biological process that starts at the early stage of wound healing，and plays a very important role in the reconstitution of the intact epidermal mechanical barrier to prevent infection and excessive moisture loss，throughout which keratinocyte migration is an essential step，and keratinocyte migration has become the focus of wound healing study．Hypoxic microenvironment is an important factor in the regulation of keratinocyte migration，but the underlying molecular mechanism is not fully elucidated As a member of Bcl一2 protein family that contains atypical BH3 domain only，BNIP3 (Bcl一2 nineteen—kilodalton interacting protein 3)is a hypoxia—reactive protein．It is well documented that BNIP3 involves in the regulation of many biological behaviors such as cell proliferation，apoptosis，autophagy and differentiation，and plays an important role in tumor development，cardiac hypertrophy and atrophy，cerebral hypoxic／ischemic damage and many other processes of disease．BNIP3 is expressed in human keratinocytes and involved in regulating their differentiation and homeostasis．But no reports were found for BNIP3 in the regulation of keratinocyte migration Upon the formation of wound，many signaling pathways are activated to mobilize wound repair cells and promote wound re—epithelialization．Focal adhesion kinase(FAK)，a cytoplasmic protein tyrosine kinase，is the core