Department of Vascular Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Department of Urology Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Mol Med Rep. 2019 Oct;20(4):3527-3534. doi: 10.3892/mmr.2019.10623. Epub 2019 Aug 27.
The present study aimed to investigate the effect of microRNA155 (miR‑155) on palmitate‑induced vascular endothelial cell injury in human umbilical vein endothelial cells (HUVECs) via the regulation of the Wnt signaling pathway. HUVECs were treated with 0.1 mM palmitate. After transfection with mimic, antagomir or the Wnt pathway inhibitor XAV939, HUVECs were divided into six treatment groups: Control, palmitate, mimic + palmitate, mimic + palmitate + XAV939, antagomir + palmitate, antagomir + palmitate + XAV939. miR‑155 expression was detected using reverse transcription‑quantitative PCR. The expression levels of the Wnt signaling pathway‑related factors β‑catenin and Cyclin D, and the inflammatory factors interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α), were detected using western blot analysis. MTT and Transwell assays were used to detect the proliferation and migration of cells, respectively. Apoptosis and reactive oxygen species (ROS) levels were determined using flow cytometry. The localization of β‑catenin in cells was determined by immunofluorescence. Palmitate reduced the expression level of miR‑155 in HUVECs. In palmitate‑induced HUVECs, overexpression of miR‑155 promoted cell proliferation, reduced the levels of apoptosis, downregulated IL‑6 and TNF‑α expression, and reduced ROS levels. Inhibition of the Wnt signaling pathway enhanced the anti‑endothelial cell injury effect caused by the overexpression of miR‑155 in palmitate‑induced HUVECs, thereby promoting proliferation, reducing apoptosis, downregulating the levels of inflammatory factors and reducing ROS levels. In summary, overexpression of miR‑155 inhibited palmitate‑induced apoptosis, ROS production and levels of inflammatory factors, and promoted the proliferation of HUVECs by negatively regulating the Wnt signaling pathway. This present study provides a theoretical basis for the prevention and treatment of cardiovascular diseases associated with endothelial cell injury.
本研究旨在探讨 microRNA155（miR-155）通过调节 Wnt 信号通路对棕榈酸诱导的人脐静脉内皮细胞（HUVEC）损伤的影响。用 0.1mM 棕榈酸处理 HUVEC。转染 mimic、antagomir 或 Wnt 通路抑制剂 XAV939 后，HUVEC 分为六组处理：对照组、棕榈酸组、mimic+棕榈酸组、mimic+棕榈酸+XAV939 组、antagomir+棕榈酸组、antagomir+棕榈酸+XAV939 组。采用逆转录定量 PCR 检测 miR-155 的表达。采用 Western blot 分析检测 Wnt 信号通路相关因子β-catenin 和 Cyclin D 以及炎症因子白细胞介素 6（IL-6）和肿瘤坏死因子-α（TNF-α）的表达水平。MTT 和 Transwell 检测分别用于检测细胞的增殖和迁移。采用流式细胞术检测细胞凋亡和活性氧（ROS）水平。通过免疫荧光检测细胞内 β-catenin 的定位。棕榈酸降低 HUVEC 中 miR-155 的表达水平。在棕榈酸诱导的 HUVEC 中，miR-155 的过表达促进细胞增殖，降低细胞凋亡水平，下调 IL-6 和 TNF-α 的表达，降低 ROS 水平。抑制 Wnt 信号通路增强了 miR-155 过表达在棕榈酸诱导的 HUVEC 中对内皮细胞损伤的拮抗作用，从而促进增殖、减少凋亡、下调炎症因子水平和降低 ROS 水平。综上所述，miR-155 的过表达通过负调控 Wnt 信号通路抑制棕榈酸诱导的细胞凋亡、ROS 生成和炎症因子水平，促进 HUVEC 的增殖。本研究为预防和治疗与内皮细胞损伤相关的心血管疾病提供了理论依据。
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