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Plasma Pattern of Extracellular Vesicles Isolated from Hepatitis C Virus Patients and Their Effects on Human Vascular
Elena Grossini1, Carlo Smirne2,3, Sakthipriyan Venkatesan1
1Laboratory of Physiology, Department of Translational Medicine, Università del Piemonte Orientale, 28100 Novara, Italy.
Insights
Extracellular vesicles (EVs) from Hepatitis C virus (HCV) patients damage blood vessel cells, contributing to cardiovascular disease (CVD) risk. Targeting inflammasomes may mitigate these harmful effects in HCV infection.
Area of Science:
- Cardiovascular Science
- Hepatology
- Cell Biology
Background:
- Hepatitis C virus (HCV) infection is linked to a higher risk of cardiovascular disease (CVD).
- Endothelial dysfunction is a key factor in the development of CVD.
Purpose of the Study:
- To investigate the role of extracellular vesicles (EVs) in causing endothelial dysfunction in Hepatitis C virus (HCV) patients.
- To explore the pathogenic mechanisms linking HCV infection, EVs, and cardiovascular disease (CVD).
Main Methods:
- Characterization of plasma EVs from 65 HCV patients with chronic liver disease.
- Stimulation of human umbilical vein endothelial cells (HUVECs) with patient-derived EVs.
- Assessment of HUVEC viability, mitochondrial membrane potential, and reactive oxygen species (ROS) production.
- Evaluation of the effects of NLRP3/AMPK and Akt pathway inhibitors.
Main Results:
- EVs from HCV patients, primarily of endothelial and lymphocyte origin, reduced HUVEC viability and mitochondrial membrane potential.
- HCV-derived EVs significantly increased ROS release in HUVECs.
- Pretreatment with NLRP3/AMPK and Akt pathway blockers attenuated the detrimental effects of EVs on HUVECs.
Conclusions:
- Circulating EVs in HCV patients can induce endothelial damage, representing a novel pathogenic mechanism for increased CVD risk.
- These findings highlight a potential therapeutic target for managing cardiovascular complications in HCV infection.
- Understanding EV-mediated pathogenesis is crucial, especially with the widespread use of antiviral therapies.
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.
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