叉头盒子A1通过激活皮肤伤口愈合中的S100A8 / p38 MAPK轴诱导血管生成
Zhongzhi Zhou1, Meilin Zou1, Hongping Chen1
1Department of Burn Plastic Surgery, The First Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, P. R. China.
Immunopharmacology and immunotoxicology
|July 17, 2023
概括
叉头盒A1 (FOXA1) 激活S100结合蛋白A8 (S100A8) 转录,促进血管生成和增强皮肤伤口愈合. 这一途径涉及p38 MAPK激活,对于这些过程至关重要.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 皮肤病学 皮肤病学
背景情况:
- S100结合蛋白A8 (S100A8) 与血管生成有关.
- 这项研究调查了S100A8在人类皮肤微血管内皮细胞 (HDMEC) 血管生成和小鼠皮肤伤口愈合中的作用.
研究的目的:
- 阐明S100A8在血管生成和皮肤伤口愈合中的功能.
- 确定参与这些过程的S100A8上游调节器.
主要方法:
- 使用GSE83582数据集进行基因表达分析.
- 用S100A8进行HDMEC传染,用于增殖,迁移和血管新生分析.
- 用腺病毒治疗进行基因变异分析的小鼠伤口模型.
- 生物信息学,露西法酶和免疫沉测试以确定上游调节者.
- 救援实验以验证FOXA1-S100A8相互作用和p38 MAPK通路.
主要成果:
- S100A8上调增强了HDMEC的增殖,迁移和血管生成,以及p38 MAPK的酸化.
- 分叉头盒A1 (FOXA1) 被确定为S100A8.8.1的上游调节器.
- 过度表达FOXA1促进了血管新生和细胞活性,其作用被S100A8抑制阻断.
- 在体内研究表明,FOXA1加速了伤口愈合,而S100A8推迟了伤口愈合.
结论:
- FOXA1通过转录激活S100A8,导致p38 MAPK酸化.
- 这个FOXA1-S100A8-p38 MAPK轴对于诱导血管生成和促进皮肤伤口愈合至关重要.
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