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1
[Study on visfatin-induced inflammation and necroptosis via LOX-1 in human umbilical vein endothelial cells].脂联素通过LOX-1诱导人脐静脉内皮细胞炎症和坏死性凋亡的研究
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2020 Oct 25;37(5):834-841. doi: 10.7507/1001-5515.202003067.
2
Visfatin stimulates production of monocyte chemotactic protein-1 and interleukin-6 in human vein umbilical endothelial cells.内脂素刺激人脐静脉内皮细胞产生单核细胞趋化蛋白-1和白细胞介素-6。
Horm Metab Res. 2009 Apr;41(4):281-6. doi: 10.1055/s-0028-1102914. Epub 2008 Nov 13.
3
The role of heat shock protein 27 phosphorylation in the proliferation and apoptosis of human umbilical vein endothelial cells induced by Visfatin.热休克蛋白27磷酸化在内脂素诱导的人脐静脉内皮细胞增殖和凋亡中的作用
Microvasc Res. 2019 Jan;121:30-36. doi: 10.1016/j.mvr.2018.08.003. Epub 2018 Aug 23.
4
[Visfatin promotes production of monocyte chemotactic protein-1 and interleukin-6 in human endothelial cells via insulin receptor].[内脂素通过胰岛素受体促进人内皮细胞中单核细胞趋化蛋白-1和白细胞介素-6的产生]
Zhonghua Yi Xue Za Zhi. 2009 Nov 3;89(40):2843-6.
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Visfatin-induced expression of inflammatory mediators in human endothelial cells through the NF-kappaB pathway.内脂素通过 NF-κB 通路诱导人内皮细胞中炎症介质的表达。
Int J Obes (Lond). 2009 Apr;33(4):465-72. doi: 10.1038/ijo.2009.24. Epub 2009 Feb 17.
6
TLR4/NF-κB signaling pathway-mediated and oxLDL-induced up-regulation of LOX-1, MCP-1, and VCAM-1 expressions in human umbilical vein endothelial cells.TLR4/NF-κB信号通路介导且氧化型低密度脂蛋白诱导人脐静脉内皮细胞中凝集素样氧化型低密度脂蛋白受体-1（LOX-1）、单核细胞趋化蛋白-1（MCP-1）和血管细胞黏附分子-1（VCAM-1）表达上调。
Genet Mol Res. 2014 Jan 28;13(1):680-95. doi: 10.4238/2014.January.28.13.
7
Ellagic acid inhibits oxidized LDL-mediated LOX-1 expression, ROS generation, and inflammation in human endothelial cells.鞣花酸可抑制氧化型 LDL 介导的人内皮细胞 LOX-1 表达、ROS 生成和炎症反应。
J Vasc Surg. 2010 Nov;52(5):1290-300. doi: 10.1016/j.jvs.2010.04.085. Epub 2010 Aug 8.
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Galectin-3 aggravates ox-LDL-induced endothelial dysfunction through LOX-1 mediated signaling pathway.半乳糖凝集素-3 通过 LOX-1 介导的信号通路加重 ox-LDL 诱导的内皮功能障碍。
Environ Toxicol. 2019 Jul;34(7):825-835. doi: 10.1002/tox.22750. Epub 2019 Apr 9.
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Ginkgolide B ameliorates oxidized low-density lipoprotein-induced endothelial dysfunction via modulating Lectin-like ox-LDL-receptor-1 and NADPH oxidase 4 expression and inflammatory cascades.银杏内酯 B 通过调节凝集素样氧化型低密度脂蛋白受体-1 和 NADPH 氧化酶 4 的表达及炎症级联反应改善氧化型低密度脂蛋白诱导的内皮功能障碍。
Phytother Res. 2018 Dec;32(12):2417-2427. doi: 10.1002/ptr.6177. Epub 2018 Aug 22.
10
Visfatin as a novel mediator released by inflamed human endothelial cells.内脏脂肪素作为一种由人内皮细胞炎症释放的新型介质。
PLoS One. 2013 Oct 10;8(10):e78283. doi: 10.1371/journal.pone.0078283. eCollection 2013.

本文引用的文献

1
Necroptosis mediated by impaired autophagy flux contributes to adverse ventricular remodeling after myocardial infarction.自噬流障碍介导的细胞坏死在心肌梗死后不良心室重构中起作用。
Biochem Pharmacol. 2020 May;175:113915. doi: 10.1016/j.bcp.2020.113915. Epub 2020 Mar 14.
2
The role of the adipocytokines vaspin and visfatin in vascular endothelial function and insulin resistance in obese children.脂联素和内脂素在肥胖儿童血管内皮功能和胰岛素抵抗中的作用。
BMC Endocr Disord. 2019 Nov 26;19(1):127. doi: 10.1186/s12902-019-0452-6.
3
Caspase-8 is the molecular switch for apoptosis, necroptosis and pyroptosis.半胱天冬酶-8 是细胞凋亡、坏死性凋亡和细胞焦亡的分子开关。
Nature. 2019 Nov;575(7784):683-687. doi: 10.1038/s41586-019-1770-6. Epub 2019 Nov 20.
4
Atherosclerosis.动脉粥样硬化。
Nat Rev Dis Primers. 2019 Aug 16;5(1):56. doi: 10.1038/s41572-019-0106-z.
5
The Coming Decade of Cell Death Research: Five Riddles.细胞死亡研究的未来十年：五个未解之谜。
Cell. 2019 May 16;177(5):1094-1107. doi: 10.1016/j.cell.2019.04.024.
6
The role of visfatin in pathogenesis of gestational diabetes (GDM).内脂素在妊娠期糖尿病（GDM）发病机制中的作用。
Ginekol Pol. 2018;89(9):518-521. doi: 10.5603/GP.a2018.0088.
7
Research Progress on the Relationship between Atherosclerosis and Inflammation.动脉粥样硬化与炎症关系的研究进展。
Biomolecules. 2018 Aug 23;8(3):80. doi: 10.3390/biom8030080.
8
Fluid shear stress regulates the expression of Lectin-like oxidized low density lipoprotein receptor-1 via KLF2-AP-1 pathway depending on its intensity and pattern in endothelial cells.流体切应力通过 KLF2-AP-1 通路调节内皮细胞中 Lectin-like 氧化型低密度脂蛋白受体-1 的表达，其表达强度和模式取决于流体切应力。
Atherosclerosis. 2018 Mar;270:76-88. doi: 10.1016/j.atherosclerosis.2018.01.038. Epub 2018 Jan 31.
9
Visfatin Promotes IL-6 and TNF-α Production in Human Synovial Fibroblasts by Repressing miR-199a-5p through ERK, p38 and JNK Signaling Pathways.内脂素通过 ERK、p38 和 JNK 信号通路抑制 miR-199a-5p 表达促进人滑膜成纤维细胞产生 IL-6 和 TNF-α。
Int J Mol Sci. 2018 Jan 8;19(1):190. doi: 10.3390/ijms19010190.
10
Expression of LOX-1 in human mesangial cells is increased by Ox-LDL and IL-1β treatment.氧化低密度脂蛋白（Ox-LDL）和白细胞介素-1β（IL-1β）处理可增加人肾小球系膜细胞中凝集素样氧化低密度脂蛋白受体-1（LOX-1）的表达。
Exp Ther Med. 2017 Oct;14(4):3632-3636. doi: 10.3892/etm.2017.4950. Epub 2017 Aug 16.

脂联素通过LOX-1诱导人脐静脉内皮细胞炎症和坏死性凋亡的研究

[Study on visfatin-induced inflammation and necroptosis via LOX-1 in human umbilical vein endothelial cells].

作者信息

Han Xiaoyu, Wu Wenchao, Liu Xiaojing, Zhu Ye

机构信息

Geriatrics Department, Chengdu Second People's Hospital, Chengdu 610017, P.R.China;Laboratory of Cardiovascular Diseases, West China Hospital, Sichuan University, Chengdu 610041, P.R.China.

Laboratory of Cardiovascular Diseases, West China Hospital, Sichuan University, Chengdu 610041, P.R.China.

出版信息

Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2020 Oct 25;37(5):834-841. doi: 10.7507/1001-5515.202003067.

DOI:10.7507/1001-5515.202003067
PMID:33140607
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10320536/
Abstract

The aim of the study is to identify the effects and underlying mechanisms of visfatin on inflammation and necroptosis in vascular endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with visfatin or pretreated with Polyinosinic acid (LOX-1 inhibitor). By using the Western blot, RT-PCR, immunocytochemistry, enzyme-linked immunosorbent assay (ELISA), MTT and flow cytometry technique, the occurrence of inflammation and necroptosis in HUVECs were evaluated. Our results showed that 100 ng/mL visfatin significantly increased the mRNA and protein expression of monocyte chemotactic protein 1 (MCP-1) and LOX-1 after 24 hours' treatment in HUVECs. However, pretreatment with Polyinosinic acid could significantly reduce the expression of MCP-1 compared with visfatin group. Additionally, 100 ng/mL visfatin could induce the production of necrotic features and increase the mRNA expression of BMF (one of the markers of necroptosis), while pretreating with Polyinosinic acid markedly downregulated the mRNA expression of BMF gene and promoted the cell proliferation. These results indicate that visfatin might induce inflammation and necroptosis via LOX-1 in HUVECs, suggesting that visfatin plays a central role in the development of atherosclerosis.

摘要

本研究的目的是确定内脂素对血管内皮细胞炎症和坏死性凋亡的影响及其潜在机制。用人内脂素刺激人脐静脉内皮细胞（HUVECs），或用聚肌苷酸（LOX-1抑制剂）进行预处理。通过蛋白质免疫印迹法、逆转录-聚合酶链反应、免疫细胞化学、酶联免疫吸附测定（ELISA）、MTT法和流式细胞术技术，评估HUVECs中炎症和坏死性凋亡的发生情况。我们的结果显示，在HUVECs中用100 ng/mL内脂素处理24小时后，单核细胞趋化蛋白1（MCP-1）和LOX-1的mRNA和蛋白表达显著增加。然而，与内脂素组相比，用聚肌苷酸预处理可显著降低MCP-1的表达。此外，100 ng/mL内脂素可诱导坏死特征的产生并增加坏死性凋亡标志物之一的BMF的mRNA表达，而用聚肌苷酸预处理可显著下调BMF基因的mRNA表达并促进细胞增殖。这些结果表明，内脂素可能通过LOX-1在HUVECs中诱导炎症和坏死性凋亡，提示内脂素在动脉粥样硬化的发展中起核心作用。