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肿瘤坏死因子-α与ERK信号通路驱动培养的人冠状动脉内皮细胞在缺氧反应中表达趋化素。

Tumor Necrosis Factor-Alpha and the ERK Pathway Drive Chemerin Expression in Response to Hypoxia in Cultured Human Coronary Artery Endothelial Cells.

作者信息

Chua Su-Kiat, Shyu Kou-Gi, Lin Yuh-Feng, Lo Huey-Ming, Wang Bao-Wei, Chang Hang, Lien Li-Ming

机构信息

Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Division of Cardiology, Department of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.

出版信息

PLoS One. 2016 Oct 28;11(10):e0165613. doi: 10.1371/journal.pone.0165613. eCollection 2016.

DOI:10.1371/journal.pone.0165613
PMID:27792771
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5085022/
Abstract

BACKGROUND

Chemerin, a novel adipokine, plays a role in the inflammation status of vascular endothelial cells. Hypoxia causes endothelial-cell proliferation, migration, and angiogenesis. This study was aimed at evaluating the protein and mRNA expression of chemerin after exposure of human coronary artery endothelial cells (HCAECs) to hypoxia.

METHODS AND RESULTS

Cultured HCAECs underwent hypoxia for different time points. Chemerin protein levels increased after 4 h of hypoxia at 2.5% O2, with a peak of expression of tumor necrosis factor-alpha (TNF-alpha) at 1 h. Both hypoxia and exogenously added TNF-alpha during normoxia stimulated chemerin expression, whereas an ERK inhibitor (PD98059), ERK small interfering RNA (siRNA), or an anti-TNF-alpha antibody attenuated the chemerin upregulation induced by hypoxia. A gel shift assay indicated that hypoxia induced an increase in DNA-protein binding between the chemerin promoter and transcription factor SP1. A luciferase assay confirmed an increase in transcriptional activity of SP1 on the chemerin promoter during hypoxia. Hypoxia significantly increased the tube formation and migration of HCAECs, whereas PD98059, the anti-TNF-alpha antibody, and chemerin siRNA each attenuated these effects.

CONCLUSION

Hypoxia activates chemerin expression in cultured HCAECs. Hypoxia-induced chemerin expression is mediated by TNF-alpha and at least in part by the ERK pathway. Chemerin increases early processes of angiogenesis by HCAECs after hypoxic treatment.

摘要

背景

chemerin是一种新型脂肪因子，在血管内皮细胞的炎症状态中发挥作用。缺氧会导致内皮细胞增殖、迁移和血管生成。本研究旨在评估人冠状动脉内皮细胞（HCAECs）暴露于缺氧环境后chemerin的蛋白质和mRNA表达。

方法与结果

培养的HCAECs在不同时间点经历缺氧。在2.5%氧气浓度下缺氧4小时后，chemerin蛋白水平升高，肿瘤坏死因子-α（TNF-α）在1小时达到表达峰值。缺氧以及常氧状态下外源性添加TNF-α均刺激chemerin表达，而ERK抑制剂（PD98059）、ERK小干扰RNA（siRNA）或抗TNF-α抗体减弱了缺氧诱导的chemerin上调。凝胶迁移试验表明，缺氧诱导chemerin启动子与转录因子SP1之间的DNA-蛋白质结合增加。荧光素酶试验证实缺氧期间SP1对chemerin启动子的转录活性增加。缺氧显著增加了HCAECs的管腔形成和迁移，而PD98059、抗TNF-α抗体和chemerin siRNA均减弱了这些作用。

结论

缺氧激活培养的HCAECs中chemerin的表达。缺氧诱导的chemerin表达由TNF-α介导，至少部分通过ERK途径介导。Chemerin增加了缺氧处理后HCAECs血管生成的早期过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/ed8e9a445c77/pone.0165613.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/ec24adff58cb/pone.0165613.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/eacb8d7c8d45/pone.0165613.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/4724f5733f9d/pone.0165613.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/ed8e9a445c77/pone.0165613.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/ec24adff58cb/pone.0165613.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/1df2c4c5ca70/pone.0165613.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/984bd22144c2/pone.0165613.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/eacb8d7c8d45/pone.0165613.g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b323/5085022/ed8e9a445c77/pone.0165613.g006.jpg

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