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人类凯瑟利西丁LL-37诱导了内皮细胞到介质细胞的过渡

Kaori Suzuki^1,2, Mari Ohkuma¹, Isao Nagaoka^1,2,3

¹Department of Host Defense and Biochemical Research, Juntendo University Graduate School of Medicine, Tokyo, Japan.

Bioscience, biotechnology, and biochemistry

|July 21, 2025

概括

抗微生物LL-37促进人体细胞内皮质转化为介质细胞 (EndMT). 这一过程涉及动脉样硬化,涉及LL-37激活Akt和NF-κB信号通路.

科学领域:

心血管生物学心血管生物学
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

内皮转介质转换 (EndMT) 是一个细胞过程,与动脉样硬化病原有关.
在动脉样硬化斑块中发现了一种抗微生物,LL-37,这表明它可能在疾病中起作用.

研究的目的:

研究LL-37在人类静脉内皮细胞 (ECs) 中诱导EndMT的潜力.
阐明LL-37介导的EndMT中涉及的信号通路.

主要方法:

用LL-37治疗人类脉EC的治疗方法.
对EC和介酶细胞标记物的评估.
评估血管网络的形成和细胞迁移.
使用Akt和NF-κB通路抑制剂的抑制研究.

主要成果:

治疗LL-37降低了内皮细胞标记物和增加了介质细胞标记物.
LL-37减少了血管网络的形成,但增强了细胞迁移.
LL-37诱导的EndMT被Akt和NF-κB途径抑制剂显著抑制.

结论:

在人体EC中,LL-37作为EndMT的诱导剂.
LL-37可能通过激活Akt和NF-κB信号通路来促进EndMT.
通过EndMT诱导,LL-37可能在动脉样硬化的发病过程中发挥作用.

关键词:

抗微生物是一种抗微生物.动脉样硬化是一种动脉样硬化.内皮细胞是内皮细胞.内皮细胞到介质细胞的过渡.在LL-37中,我们可以看到LL-37.

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