IL-13 neutralization attenuates carotid artery intimal hyperplasia and increases endothelial cell migration via modulating the JAK-1/STAT-3 signaling pathway.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2023-12-01 Epub Date: 2023-10-09 DOI:10.1080/19336918.2023.2265158
Qi Li, Yue Li, Fengjiao Wu, Jingyu Li, Zhongsha Li, Xiaoling Qin, Simeng Wei, Chang Chen
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引用次数: 0

Abstract

The aim of this study was to investigate how the concentration of interleukin-13 (IL-13) affects the regulation of endothelial cell migration after injury. The incubation of recombinant human interleukin-13 (rhIL-13) strongly increased the content of reactive oxygen species (ROS) in HUVECs via the JAK-1/STAT-3/NOX-4 signaling pathway. Antagonizing the high intracellular ROS that was induced by rhIL-13 promoted the migration of HUVECs. Furthermore, IL-13 neutralization not only inhibited intimal hyperplasia, but also promoted the migration of endothelial cells (ECs) after injury. The results suggest that IL-13 inhibition is a potential means of stimulating endothelial cells recovery after injury. Therefore, the attenuation of IL-13 activation may have therapeutic value for vascular disease.

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IL-13中和通过调节JAK-1/STAT-3信号通路减轻颈动脉内膜增生并增加内皮细胞迁移。
本研究的目的是研究白细胞介素13(IL-13)的浓度如何影响损伤后内皮细胞迁移的调节。重组人白细胞介素13(rhIL-13)的孵育通过JAK-1/STAT-3/NOX-4信号通路显著增加HUVECs中活性氧(ROS)的含量。拮抗rhIL-13诱导的高细胞内ROS促进了HUVECs的迁移。此外,IL-13的中和不仅抑制了内膜增生,而且促进了损伤后内皮细胞的迁移。结果表明,抑制IL-13是刺激损伤后内皮细胞恢复的一种潜在手段。因此,IL-13激活的减弱可能对血管疾病具有治疗价值。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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