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首页> 外文期刊>Cell biology international. >CRISPR‐Cas9 mediated gene knockout in human coronary artery endothelial cells reveals a pro‐inflammatory role of TLR2
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CRISPR‐Cas9 mediated gene knockout in human coronary artery endothelial cells reveals a pro‐inflammatory role of TLR2

机译：CRISPR-CAS9介导的人冠状动脉内皮细胞中的基因敲除揭示了TLR2的促炎症作用

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摘要

Abstract Endothelial inflammatory responses promote the development and progression of atherosclerosis. It was reported that Toll‐like receptors 2 (TLR2) is associated with endothelial inflammation. However, the effect of TLR2 on inflammatory responses in human coronary artery endothelial cells (HCAECs) remains largely unknown. Here, we tested the hypothesis that TLR2 can enhance inflammatory reactions in HCAECs after stimulated by TLR2 agonist. First, we used CRISPR‐Cas9 technology to knockout TLR2 gene in HCAECs. Then, TLR2‐KO and wild type HCAECs were treated with TLR2 agonist peptidoglycan (PGN). The expression levels of intercellular cell adhesion molecule‐1 (ICAM‐1), interleukin‐6 (IL‐6), and interleukin‐8 (IL‐8) were analyzed by real‐time PCR, Western blot, and ELISA. The expression status of myeloid differentiation primary response gene 88 (MyD88), phosphorylated IRAK‐1 (pIRAK‐1) and phosphorylated NF‐κB (pNF‐κB) were detected by Western blot. Our results show that after treated with TLR2 agonist, the expression levels of ICAM‐1, IL‐6, and IL‐8 were downregulated in TLR2‐KO cells compared to those of wild type cells. Further, Western blots of MyD88, pIRAK‐1, and pNF‐κB show that the expression levels of these pro‐inflammatory molecules were much lower in TLR2‐KO cells compared to that of wild type cells by stimulating with TLR2 agonist. We suggest that TLR2 may affect inflammatory reaction in HCAECs by introducing pro‐inflammatory molecules like MyD88, pIRAK‐1, and pNF‐κB.
机译：摘要内皮炎症反应促进动脉粥样硬化的发展和进展。据报道，Toll样受体2（TLR2）与内皮炎症有关。然而，TLR2对人冠状动脉内皮细胞（HCAECs）中炎症反应的影响仍然很大程度上。在这里，我们测试了TLR2在TLR2激动剂刺激后TLR2可以在HCAEC中提高炎症反应。首先，我们使用CRISPR-CAS9技术在HCAECS中敲除TLR2基因。然后，用TLR2激动剂肽聚糖（PGN）处理TLR2-KO和野生型HCAEC。通过实时PCR，Western印迹和ELISA分析细胞间粘附分子-1（ICAM-1），白细胞介素-6（IL-8）和白细胞介素-8（IL-8）的表达水平。蛋白质印迹检测髓样分化初级反应基因88（MYD88），磷酸化的伊拉克-1（PRAK-1）和磷酸化NF-κB（PNF-κB）的表达状态。我们的研究结果表明，用TLR2激动剂处理后，与野生型细胞相比，在TLR2-KO细胞中下调ICAM-1，IL-6和IL-8的表达水平。此外，MyD88，Pirak-1和PNF-κB的Western印迹表明，通过用TLR2激动剂刺激通过刺激野生型细胞，这些促炎分子的表达水平在TLR2-KO细胞中得多。我们认为TLR2可以通过引入像myD88，Pirak-1和PNF-κB等促炎症分子来影响HCAEC中的炎症反应。

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  • 来源
    《Cell biology international.》 |2018年第2期|共7页
  • 作者

    Wang Yingge; Chen Lu; Tian Zheng; Shen Xueyi; Wang Xiaohong; Wu Honghai; Wang Yayi; Zou Jiayu; Liang Jingyan;

  • 作者单位

    The Department of Neurology Affiliated Hospital of Yangzhou UniversityYangzhou UniversityYangzhou;

    Research Center for Vascular Biology College of MedicineYangzhou UniversityYangzhou China;

    The Department of Cardiology Affiliated Zhongshan Hospital of Dalian UniversityDalianChina;

    Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and;

    Research Center for Vascular Biology College of MedicineYangzhou UniversityYangzhou China;

    Research Center for Vascular Biology College of MedicineYangzhou UniversityYangzhou China;

    Research Center for Vascular Biology College of MedicineYangzhou UniversityYangzhou China;

    Research Center for Vascular Biology College of MedicineYangzhou UniversityYangzhou China;

    Research Center for Vascular Biology College of MedicineYangzhou UniversityYangzhou China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    atherogenesis; coronary artery endothelial cell; CRISPR‐Cas9; inflammatory; TLR2;

    机译：血液发生;冠状动脉内皮细胞;CRISPR-CAS9;炎症;TLR2;

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