The role of PPARγ in intermittent hypoxia-related human umbilical vein endothelial cell injury,Sleep and Breathing

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The role of PPARγ in intermittent hypoxia-related human umbilical vein endothelial cell injury
Sleep and Breathing ( IF 2.1 ) Pub Date : 2022-08-09 , DOI: 10.1007/s11325-022-02696-x
Lian Ning-Fang ₁ , Jin Yong-Xu ₁ , Chen Jia ₁ , Wang Cai-Yun ₁ , Huang Jie-Feng ₁ , Lin Qi-Chang ₁

Affiliation

Purpose

Patients with obstructive sleep apnoea (OSA) have a high incidence of vascular endothelial injury. The most important pathophysiological feature of OSA is chronic intermittent hypoxia (CIH). This study aimed to investigate the mechanisms of CIH-related vascular endothelial injury.

Methods

IH exposure was applied to human umbilical vein endothelial cells (HUVECs). After modeling, cell viability, the expression levels of peroxisome proliferator activated receptor γ (PPARγ), apoptosis-associated proteins and mitochondrial division fusion proteins, and the levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were assessed via Cell Counting Kit-8 (CCK-8), western blotting, fluorescent microscope, and flow cytometry, respectively. Rosiglitazone (PPARγ agonist), tempo (the mitochondrial-specific antioxidant), and tempo combined with PPARγ interfering RNA were used to treat HUVECs, respectively.

Results

After IH exposure, cell viability and levels of MMP decreased, cell apoptosis and ROS levels increased, and the expression levels of PPARγ decreased. Both tempo and rosiglitazone pretreatment ameliorated cell apoptosis and improved cell viability. In addition, mitochondrial function became better after tempo pretreatment. PPARγ interference reversed the protective effects of tempo on IH-related mitochondrial function injury and cell injury.

Conclusions

PPARγ regulated the apoptosis and cell viability of IH-treated HUVECs by altering mitochondrial function. This finding clarifies the mechanism of CIH-related vascular endothelial injury.

中文翻译：

PPARγ在间歇性缺氧相关人脐静脉内皮细胞损伤中的作用

目的

阻塞性睡眠呼吸暂停 (OSA) 患者血管内皮损伤的发生率很高。OSA最重要的病理生理特征是慢性间歇性缺氧（CIH）。本研究旨在探讨 CIH 相关血管内皮损伤的机制。

方法

IH 暴露应用于人脐静脉内皮细胞 (HUVEC)。建模后，通过 Cell 评估细胞活力、过氧化物酶体增殖物激活受体 γ (PPARγ)、凋亡相关蛋白和线粒体分裂融合蛋白的表达水平，以及活性氧 (ROS) 和线粒体膜电位 (MMP) 的水平分别为 Counting Kit-8 (CCK-8)、western blotting、荧光显微镜和流式细胞仪。罗格列酮（PPARγ 激动剂）、tempo（线粒体特异性抗氧化剂）和 tempo 结合 PPARγ 干扰 RNA 分别用于治疗 HUVEC。