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COL8A1在炎症性内皮细胞到介质细胞过渡过程中调节内皮细胞表型

Qian Li¹, Lifang Ye^1,2, Sriharsha Talapaneni¹

¹Department of Medicine, University of California, Los Angeles, California, United States.

American journal of physiology. Heart and circulatory physiology

|October 3, 2025

概括

原蛋白8型α1链 (COL8A1) 在血管疾病中起着双重作用. 它的早期抑制促进了内皮细胞到介质细胞的过渡 (EndMT),而后来的上调反映了疾病的进展,表明了治疗潜力.

科学领域:

血管生物学血管生物学
细胞生物学细胞生物学
病理学病理学病理学

背景情况:

内皮转介质转换 (EndMT) 与诸如动脉样硬化等炎症性血管疾病有关.
尽管原蛋白 VIII 型α 1 链 (COL8A1) 参与了动脉动脉生成,但其在EndMT中的作用尚不清楚.

研究的目的:

为了研究COL8A1在炎症EndMT中的作用.
为了确定COL8A1在炎症应激下内皮细胞稳定性的功能.

主要方法:

对暴露于异构刺激的内皮细胞进行单细胞RNA-seq分析.
在小鼠动脉样硬化病变中的免疫光.
在体外研究中,使用人类大动脉内皮细胞 (HAEC) 治疗TNF-α,COL8A1过度表达或siRNA抑制.

主要成果:

在动脉样硬化病变和长期TNF-α治疗后的HAEC中,COL8A1表达增加.
短期TNF-α治疗降低了COL8A1的调节,抑制了内皮基因程序,并通过NF-κB/Snail信号传输促进了EndMT.
COL8A1过度表达或添加保存了内皮标记物和减弱的TNF-α诱导的EndMT.

结论:

在炎症期间,COL8A1作为内皮稳定性的关键调节者.
暂时的COL8A1抑制促进了早期的EndMT,而后来的诱导反映了疾病的重塑.
COL8A1被确定为血管疾病的潜在生物标志物和治疗标.

关键词:

在 COL8A1 中使用.第八种类型的原蛋白内皮细胞到介质细胞的过渡.这是一种炎症炎症炎症炎症.瘤丧亡因子α因子

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