颗粒物增加了连接素43的表达,并加剧了内皮屏障破坏
Jun Zhang1,2, Xiaomin Wu1, Ying Liang1
1Department of Medicine, University of Arizona Tuscon, AZ, USA.
American journal of translational research
|September 11, 2023
概括
颗粒物空气污染增加了肺细胞中的联结素43 (Cx43),破坏了内皮壁垒. 抑制Cx43可能会防止污染引起的心肺损伤.
科学领域:
- 环境健康 环境健康
- 细胞生物学 细胞生物学
- 心肺研究研究 心肺研究
背景情况:
- 颗粒物 (PM) 空气污染加剧了心肺疾病.
- 暴露于颗粒物会破坏内皮细胞细胞骨架和结点.
- 颗粒物对内皮细胞-细胞通信和间隙结的影响仍然不清楚.
研究的目的:
- 为了研究联结素43 (Cx43) 在PM诱导的内皮功能障碍中的作用.
- 描述PM对肺内皮细胞 (ECs) 间隙结活动的影响.
主要方法:
- 培养的人类肺部EC被暴露在一个具有良好特征的PM样本中.
- 分析了mRNA和蛋白质水平上的Cx43表达.
- 通过染料转移和EC屏障功能使用跨内皮电阻 (TER) 评估间隙结活动.
主要成果:
- 暴露于颗粒物会以时间依赖的方式增加Cx43表达,由ROS清除剂N-乙半氨酸 (NAC) 调节.
- PM在血和ER/Golgi上增加了Cx43,增加了间隙结活动,并破坏了EC屏障功能.
- Cx43抑制 (GAP27) 和敲击减弱的PM诱导的屏障破坏和肌光链 (MLC) 酸化.
结论:
- 在PM介导的内皮屏障破坏和信号传导中,Cx43是至关重要的.
- Cx43代表了PM相关心肺疾病的潜在治疗标.
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