在因高氧引起的内皮细胞损伤中自的保护作用和机制
Xiaodan Zhu1,2,3, Shasha He1,2,3, Rong Zhang1,2,3
1Division of Neonatology, Department of Pediatrics, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
American journal of perinatology
|July 29, 2023
概括
自作为一种保护机制,防止高氧诱导的内皮细胞损伤,可能通过调节FOXO1的翻译后修饰. 这一发现对于了解早产婴儿的支气管肺功能障碍症至关重要.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 新生儿生理学 新生儿生理学
背景情况:
- 支气管肺功能障碍症 (BPD) 是早产婴儿的慢性肺部疾病,其特征是气膜简化和肺血管发育受损,过氧是主要原因.
- 细胞降解过程自与氧化应激有关,已知其通过FOXO1后翻译修饰的调节.
- 自在过氧诱导的内皮细胞损伤中的特定作用尚不清楚.
研究的目的:
- 为了研究自在因高氧引起的内皮细胞损伤中的作用.
- 阐明潜在的机制,包括FOXO1的翻译后修改的参与.
主要方法:
- 人的静脉内皮细胞 (HUVEC) 经受过高氧化.
- 自被激活或抑制以评估其对细胞功能的影响.
- 分析了与自相关的蛋白质和FOXO1修饰的表达水平.
主要成果:
- 过氧症降低了自性蛋白质表达,损害了细胞迁移和管形成,增加了活性氧物种和透性.
- 自的激活减轻了高氧引起的损伤,而抑制则加剧了它.
- 减少自与增加的FOXO1酸化和乙化相关.
结论:
- 自作用对过氧诱导的内皮细胞损伤起着保护作用.
- 自可以通过FOXO1转化后修饰的共同调节来调节其保护作用.
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