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抑制ADAM17可部分通过下调GRO-α/CXCR2表达减轻高糖诱导的内皮细胞血管生成和炎症：对腹膜透析的意义

Inhibition of ADAM17 attenuates high glucose-induced angiogenesis and inflammation in endothelial cells partly through down-regulation of GRO-α/CXCR2 expression: implications in peritoneal dialysis.

作者信息

Jiang Na, Feng Hao, Xie Weizhen, Gu Leyi, Fang Wei, Ding Tingting, Yuan Jiangzi

机构信息

Department of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Ren Ji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Department of Nephrology, Baoshan Site of Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

Clin Exp Nephrol. 2024 Dec;28(12):1232-1240. doi: 10.1007/s10157-024-02546-y. Epub 2024 Sep 21.

DOI:10.1007/s10157-024-02546-y
PMID:39305454
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11621206/
Abstract

BACKGROUND

Angiogenesis and inflammation are key events leading to peritoneal morphologic alteration and ultrafiltration failure in patients undergoing peritoneal dialysis (PD). The current study aims to explore the role of ADAM17 in the angiogenetic and inflammatory responses of endothelial cells.

METHODS

Human umbilical vein endothelial cells (HUVECs) were cultured and treated with a high glucose-containing medium. In parallel experiments, the expression of ADAM17 in HUVECs was inhibited by SiRNA interference. The mRNA and protein expression of ADAM17, GRO-α and CXCR2 were assessed by qPCR and Western blotting, respectively. The concentrations of GRO-α, VEGF, IL-6 and TNF-α in the cellular supernatants were determined by ELISA. Tube formation and migration of HUVECs were evaluated by Matrigel and transwell migration apparatus.

RESULTS

High glucose increased the expression of ADAM17, CXCR2 and GRO-α in cultured HUVECs. RNA silencing of ADAM17 abolished high glucose-mediated increase of GRO-α and CXCR2, which were accompanied by reduced secretion of VEGF, IL-6, TNF-α, as well as tube formation and cell migration in HUVECs.

CONCLUSIONS

Inhibition of ADAM17 ameliorates high glucose-induced angiogenic and inflammatory responses in endothelial cells partly through down-regulation of GRO-α/CXCR2 expression.

摘要

背景

血管生成和炎症是导致腹膜透析（PD）患者腹膜形态改变和超滤失败的关键事件。本研究旨在探讨ADAM17在内皮细胞血管生成和炎症反应中的作用。

方法

培养人脐静脉内皮细胞（HUVECs）并用含高糖的培养基处理。在平行实验中，通过SiRNA干扰抑制HUVECs中ADAM17的表达。分别通过qPCR和蛋白质印迹法评估ADAM17、GRO-α和CXCR2的mRNA和蛋白质表达。通过ELISA测定细胞上清液中GRO-α、VEGF、IL-6和TNF-α的浓度。通过基质胶和Transwell迁移装置评估HUVECs的管形成和迁移。

结果

高糖增加了培养的HUVECs中ADAM17、CXCR2和GRO-α的表达。ADAM17的RNA沉默消除了高糖介导的GRO-α和CXCR2的增加，同时伴有HUVECs中VEGF、IL-6、TNF-α的分泌减少以及管形成和细胞迁移减少。

结论

抑制ADAM1部分通过下调GRO-α/CXCR2表达改善高糖诱导的内皮细胞血管生成和炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e53/11621206/41606378f3bd/10157_2024_2546_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e53/11621206/308bb009eb61/10157_2024_2546_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e53/11621206/64bb9401aa35/10157_2024_2546_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e53/11621206/711b026909bb/10157_2024_2546_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e53/11621206/41606378f3bd/10157_2024_2546_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e53/11621206/308bb009eb61/10157_2024_2546_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e53/11621206/64bb9401aa35/10157_2024_2546_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e53/11621206/711b026909bb/10157_2024_2546_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3e53/11621206/41606378f3bd/10157_2024_2546_Fig4_HTML.jpg

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本文引用的文献

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Connexin 43 (Cx43) regulates high-glucose-induced retinal endothelial cell angiogenesis and retinal neovascularization.
缝隙连接蛋白 43（Cx43）调节高糖诱导的视网膜内皮细胞血管生成和视网膜新生血管形成。
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Peritoneal Dialysis.腹膜透析
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