删除TRPC6增强了eNOS表达,并减少了LPS引起的急性肺损伤
Mengyuan Wang1,2, Xingfang Zhang2, Juan Guo1
1Institute of Medical Research, Northwestern Polytechnical University, Xi'an 710072, China.
International journal of molecular sciences
|December 9, 2023
概括
抑制短暂受体潜在通道6 (TRPC6) 通过改善内皮屏障功能和调节氧化合成酶来减少急性肺损伤 (ALI). 这一发现为ALI治疗提供了一个新的治疗点.
科学领域:
- 肺部医学 肺部医学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 急性肺损伤 (ALI) 涉及内皮壁障碍的破坏和炎症.
- 短暂受体潜在阴离子通道6 (TRPC6) 调解的流入,这对于内皮膜的超透性至关重要.
研究的目的:
- 调查TRPC6在脂聚糖 (LPS) 诱导的ALI中的作用.
- 阐明TRPC6参与内皮膜超透性和炎症的机制.
主要方法:
- 使用野生类型 (WT) 和TRPC6淘汰 (TRPC6-/-) 鼠肺中的RNA测序进行基因表达分析.
- 使用人类静脉内皮细胞 (HUVEC) 进行体外研究,以评估LPS诱导的超透性和TRPC6抑制.
- 使用拉力西尔对TRPC6的药理抑制以及对eNOS和ROS下游影响的评估.
主要成果:
- TRPC6 缺失减轻了LPS诱导的肺,并减少了炎症细胞的透.
- RNA测序揭示了TRPC6-/-肺部下调的细胞粘附分子,表明对LPS损伤的保护.
- 抑制TRPC6降低了LPS诱导的超透性,ROS产量,并恢复了HUVEC中的eNOS表达.
结论:
- 抑制TRPC6可以改善LPS诱导的ALI.
- TRPC6可以通过调节细胞粘附分子通路和内皮细胞中的eNOS水平来发挥其保护作用.
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