FN14通过通过ANXA2/ERK1/2轴调节热致死,促进呼吸器诱导的肺损伤
1Department of Respiratory and Critical Medicine, the Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China; School of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, China.
纤维细胞生长因子14 (FN14) 通过通过ANXA2/ERK1/2通路促进热致死,驱动呼吸器诱导的肺损伤 (VILI). 在VILI模型中,抑制FN14可缓解肺部损伤并降低火死.
科学领域:
- 肺部医学 肺部医学
- 炎症研究 炎症研究
- 分子生物学分子生物学
背景情况:
- 呼吸器诱导的肺损伤 (VILI) 涉及一种无法控制的炎症级联.
- 纤维细胞生长因子14 (FN14) 涉及急性炎症疾病,但其在VILI中的作用尚不清楚.
研究的目的:
- 为了阐明FN14在VILI中的机制.
- 为了研究FN14/ANXA2/ERK1/2轴在VILI诱导的烧灭中的作用.
主要方法:
- 已建立的VILI的老鼠和细胞模型.
- 使用H&E染色,qRT-PCR,西斑和免疫组织化学来评估肺损伤和蛋白质表达.
- 采用分子对接,质谱,共免疫沉和免疫光检测来验证FN14-ANXA2结合,并进行救援实验来探索FN14/ANXA2/ERK1/2轴.
主要成果:
- 在VILI模型中,FN14表达得到了上调.
- 抑制FN14可减轻肺损伤和减少烧死,而过度表达则加剧了这些影响.
- FN14增强了ANXA2的结合和酸化,激活了ERK1/2通路,导致热.
结论:
- 在VILI中,FN14被上调,并促进肺损伤.
- 通过ANXA2/ERK1/2轴,FN14调节了VILI诱导的烧.
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