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钙/ NFAT 在川崎病患者血清诱导的人冠状动脉内皮细胞功能障碍和炎症中的作用。

The role of Ca/NFAT in Dysfunction and Inflammation of Human Coronary Endothelial Cells induced by Sera from patients with Kawasaki disease.

机构信息

Department of Cardiology, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333 Binsheng Road, Hangzhou, 310052, PR China.

出版信息

Sci Rep. 2020 Mar 13;10(1):4706. doi: 10.1038/s41598-020-61667-y.

DOI:10.1038/s41598-020-61667-y
PMID:32170198
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7069934/
Abstract

Ca/nuclear factor of activated T-cells (Ca/NFAT) signaling pathway may play a crucial role in the pathogenesis of Kawasaki disease (KD). We investigated the poorly understood Ca/NFAT regulation of coronary artery endothelial cells and consequent dysfunction in KD pathogenesis. Human coronary artery endothelial cells (HCAECs) stimulated with sera from patients with KD, compared with sera from healthy children, exhibited significant increases in proliferation and angiogenesis, higher levels of NFATc1 and NFATc3 and some inflammatory molecules, and increased nuclear translocation of NFATc1 and NFATc3. HCAECs stimulated with sera from patients with KD treated with cyclosporine A (CsA) showed decreased proliferation, angiogenesis, NFATc1 and inflammatory molecules levels as compared with results for untreated HCAECs. In conclusion, our data reveal that KD sera activate the Ca/NFAT in HCAECs, leading to dysfunction and inflammation of endothelial cells. CsA has cytoprotective effects by ameliorating endothelial cell homeostasis via Ca/NFAT.

摘要

钙/激活 T 细胞核因子（Ca/NFAT）信号通路可能在川崎病（KD）的发病机制中发挥关键作用。我们研究了在 KD 发病机制中尚未充分了解的冠状动脉内皮细胞的 Ca/NFAT 调控及其随后的功能障碍。与来自健康儿童的血清相比，用来自 KD 患者的血清刺激的人冠状动脉内皮细胞（HCAEC）表现出明显的增殖和血管生成增加、更高水平的 NFATc1 和 NFATc3 以及一些炎症分子，以及 NFATc1 和 NFATc3 的核易位增加。与未处理的 HCAEC 相比，用环孢素 A（CsA）处理的来自 KD 患者的血清刺激的 HCAEC 显示增殖、血管生成、NFATc1 和炎症分子水平降低。总之，我们的数据表明，KD 血清激活 HCAEC 中的 Ca/NFAT，导致内皮细胞功能障碍和炎症。CsA 通过改善内皮细胞稳态通过 Ca/NFAT 发挥细胞保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ff1/7069934/910f1a000252/41598_2020_61667_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ff1/7069934/0da64578bad6/41598_2020_61667_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ff1/7069934/05cb734c921b/41598_2020_61667_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ff1/7069934/af7de2e840a5/41598_2020_61667_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ff1/7069934/910f1a000252/41598_2020_61667_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ff1/7069934/0da64578bad6/41598_2020_61667_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ff1/7069934/05cb734c921b/41598_2020_61667_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ff1/7069934/af7de2e840a5/41598_2020_61667_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ff1/7069934/910f1a000252/41598_2020_61667_Fig4_HTML.jpg

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