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SENP3 通过 ROS 依赖的信号通路调节高糖诱导的内皮功能障碍。

SENP3 regulates high glucose-induced endothelial dysfunction via ROS dependent signaling.

机构信息

Department of Cardiology, Shanxi Provincial People's Hospital, Taiyuan, Shanxi, China.

出版信息

Diab Vasc Dis Res. 2020 Nov-Dec;17(6):1479164120970895. doi: 10.1177/1479164120970895.

DOI:10.1177/1479164120970895
PMID:33231124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7919223/
Abstract

BACKGROUND

The current study aimed to explore the role of SENP3 in endothelial cell dysfunction in a high-glucose setting.

METHODS

The gene and protein expressions of SENP3 in high-glucose cultured HAECs were examined using quantitative PCR and western blotting. The effects of SENP3 on HAEC viability, apoptosis, migration, and endothelial-monocyte adhesion were evaluated in vitro by knockdown. Moreover, a mouse streptozotocin-induced type I diabetes model was established for SENP3 expression assessment. In addition, the effects of SENP3 on ROS-related signaling pathways were investigated in high-glucose cultured HAECs.

RESULTS

Significantly increased levels of SENP3 mRNA and protein were found in high-glucose cultured HAECs in a time-dependent manner. SENP3 knockdown reversed high glucose-induced HAEC viability, apoptosis, and migration reduction. SENP3 knockdown attenuated the high glucose-induced intercellular adhesion of THP-1 monocytic cells and HAECs via downregulation of ICAM-1 and VCAM-1 expression. Increased levels of SENP3, ICAM-1, and VCAM-1 expression were observed in the aorta tissue of mice with type I diabetes. Downregulation of SENP3 expression was observed in HAECs cultured with high glucose levels using the free radical scavenger N-acetyl-L-cysteine or NOX4 siRNA.

CONCLUSIONS

SENP3 was involved in high glucose-induced endothelial dysfunction, and ROS-dependent signaling served as the mechanism.

摘要

背景

本研究旨在探讨 SENP3 在高糖环境下内皮细胞功能障碍中的作用。

方法

采用实时定量 PCR 和 Western blot 检测高糖培养的人脐静脉内皮细胞（HAECs）中 SENP3 的基因和蛋白表达。通过敲低 SENP3 评估其对 HAEC 活力、凋亡、迁移和内皮细胞-单核细胞黏附的影响。此外，建立了小鼠链脲佐菌素诱导的 1 型糖尿病模型，以评估 SENP3 的表达。还研究了 SENP3 在高糖培养的 HAECs 中对 ROS 相关信号通路的影响。

结果

高糖培养的 HAECs 中 SENP3 的 mRNA 和蛋白水平呈时间依赖性增加。SENP3 敲低逆转了高糖诱导的 HAEC 活力、凋亡和迁移减少。SENP3 敲低通过下调 ICAM-1 和 VCAM-1 的表达，减弱了高糖诱导的 THP-1 单核细胞和 HAEC 之间的细胞间黏附。1 型糖尿病小鼠主动脉组织中 SENP3、ICAM-1 和 VCAM-1 的表达水平增加。在高糖培养的 HAECs 中，使用自由基清除剂 N-乙酰-L-半胱氨酸或 NOX4 siRNA 下调 SENP3 表达。

结论

SENP3 参与了高糖诱导的内皮功能障碍，ROS 依赖性信号通路是其作用机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/c4711d546f8c/10.1177_1479164120970895-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/91d85dfac894/10.1177_1479164120970895-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/d500a84417ab/10.1177_1479164120970895-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/b0ae48d10657/10.1177_1479164120970895-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/b90b47bda24a/10.1177_1479164120970895-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/c4711d546f8c/10.1177_1479164120970895-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/91d85dfac894/10.1177_1479164120970895-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/d500a84417ab/10.1177_1479164120970895-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/b0ae48d10657/10.1177_1479164120970895-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/b90b47bda24a/10.1177_1479164120970895-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05ed/7919223/c4711d546f8c/10.1177_1479164120970895-fig5.jpg

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本文引用的文献

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2
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J Clin Med. 2019 Nov 2;8(11):1856. doi: 10.3390/jcm8111856.
3
The role of post-translational modifications in cardiac hypertrophy.翻译后修饰在心肌肥大中的作用。
纳米姜黄素可减轻高糖和颗粒物诱导的内皮炎症：线粒体功能及 miR-221/222 的作用。
Int J Nanomedicine. 2023 Dec 6;18:7379-7402. doi: 10.2147/IJN.S433658. eCollection 2023.
4
Nox4 as a novel therapeutic target for diabetic vascular complications.Nox4 作为糖尿病血管并发症的一个新的治疗靶点。
Redox Biol. 2023 Aug;64:102781. doi: 10.1016/j.redox.2023.102781. Epub 2023 Jun 9.
5
SENP3 Aggravates Renal Tubular Epithelial Cell Apoptosis in Lipopolysaccharide-Induced Acute Kidney Injury via deSUMOylation of Drp1.SENP3通过去SUMO化Drp1加重脂多糖诱导的急性肾损伤中的肾小管上皮细胞凋亡。
Kidney Dis (Basel). 2022 Jun 30;8(5):424-435. doi: 10.1159/000525308. eCollection 2022 Nov.
6
Effect of Platelet-Derived Growth Factor C on Mitochondrial Oxidative Stress Induced by High d-Glucose in Human Aortic Endothelial Cells.血小板衍生生长因子C对高糖诱导的人主动脉内皮细胞线粒体氧化应激的影响。
Pharmaceuticals (Basel). 2022 May 23;15(5):639. doi: 10.3390/ph15050639.
J Cell Mol Med. 2019 Jun;23(6):3795-3807. doi: 10.1111/jcmm.14330. Epub 2019 Apr 4.
4
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5
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6
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7
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9
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10
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