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从丙型肝炎病毒患者中分离出的细胞外囊泡的血浆模式及其对人血管内皮细胞的影响。

Plasma Pattern of Extracellular Vesicles Isolated from Hepatitis C Virus Patients and Their Effects on Human Vascular Endothelial Cells.

机构信息

Laboratory of Physiology, Department of Translational Medicine, Università del Piemonte Orientale, 28100 Novara, Italy.

Internal Medicine Unit, Department of Translational Medicine, Università del Piemonte Orientale, 28100 Novara, Italy.

出版信息

Int J Mol Sci. 2023 Jun 15;24(12):10197. doi: 10.3390/ijms241210197.

DOI:10.3390/ijms241210197
PMID:37373343
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10299492/
Abstract

Hepatitis C virus (HCV) patients are at increased risk of cardiovascular disease (CVD). In this study, we aimed to evaluate the role of extracellular vesicles (EVs) as pathogenic factors for the onset of HCV-related endothelial dysfunction. Sixty-five patients with various stages of HCV-related chronic liver disease were enrolled in this case series. Plasma EVs were characterized and used to stimulate human vascular endothelial cells (HUVEC), which were examined for cell viability, mitochondrial membrane potential, and reactive oxygen species (ROS) release. The results showed that EVs from HCV patients were mainly of endothelial and lymphocyte origin. Moreover, EVs were able to reduce cell viability and mitochondrial membrane potential of HUVEC, while increasing ROS release. Those harmful effects were reduced by the pretreatment of HUVEC with the NLR family pyrin domain containing 3 (NLRP3)/AMP-activated protein kinase and protein kinase B blockers. In conclusion, in HCV patients, we could highlight a circulating pattern of EVs capable of inducing damage to the endothelium. These data represent a novel possible pathogenic mechanism underlying the reported increase of CVD occurrence in HCV infection and could be of clinical relevance also in relation to the widespread use of antiviral drugs.

摘要

丙型肝炎病毒 (HCV) 患者患心血管疾病 (CVD) 的风险增加。在这项研究中，我们旨在评估细胞外囊泡 (EVs) 作为 HCV 相关内皮功能障碍发病因素的作用。本病例系列纳入了 65 名患有不同阶段 HCV 相关慢性肝病的患者。对血浆 EVs 进行了特征描述，并用于刺激人血管内皮细胞 (HUVEC)，检查细胞活力、线粒体膜电位和活性氧 (ROS) 的释放。结果表明，HCV 患者的 EVs 主要来源于内皮细胞和淋巴细胞。此外，EVs 能够降低 HUVEC 的细胞活力和线粒体膜电位，同时增加 ROS 的释放。这些有害影响可通过 NLR 家族包含 pyrin 结构域的 3 (NLRP3)/AMP 激活蛋白激酶和蛋白激酶 B 阻滞剂预处理 HUVEC 来减轻。总之，在 HCV 患者中，我们可以强调一种能够诱导内皮损伤的循环 EVs 模式。这些数据代表了 HCV 感染中报道的 CVD 发生率增加的一个新的可能发病机制，并且与抗病毒药物的广泛使用也具有临床相关性。

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