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内皮细胞对丙型肝炎病毒重组包膜糖蛋白2蛋白暴露的炎症反应。

Inflammatory response of endothelial cells to hepatitis C virus recombinant envelope glycoprotein 2 protein exposure.

作者信息

Urbaczek Ana Carolina, Ribeiro Lívia Carolina de Abreu, Ximenes Valdecir Farias, Afonso Ana, Nogueira Camila Tita, Generoso Wesley Cardoso, Alberice Juliana Vieira, Rudnicki Martina, Ferrer Renila, Fonseca Luiz Marcos da, Costa Paulo Inácio da

机构信息

Laboratório de Imunologia Clínica, Departamento de Análises Clínicas, Escola de Ciências Farmacêuticas, Bauru, SP, Brasil.

Departamento de Química, Faculdade de Ciências, Universidade Estadual Paulista Julio de Mesquita Filho, Bauru, SP, Brasil.

出版信息

Mem Inst Oswaldo Cruz. 2014 Sep;109(6):748-56. doi: 10.1590/0074-0276140090. Epub 2014 Sep 9.

DOI:10.1590/0074-0276140090
PMID:25317702
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4238766/
Abstract

The hepatitis C virus (HCV) encodes approximately 10 different structural and non-structural proteins, including the envelope glycoprotein 2 (E2). HCV proteins, especially the envelope proteins, bind to cell receptors and can damage tissues. Endothelial inflammation is the most important determinant of fibrosis progression and, consequently, cirrhosis. The aim of this study was to evaluate and compare the inflammatory response of endothelial cells to two recombinant forms of the HCV E2 protein produced in different expression systems (Escherichia coli and Pichia pastoris). We observed the induction of cell death and the production of nitric oxide, hydrogen peroxide, interleukin-8 and vascular endothelial growth factor A in human umbilical vein endothelial cells (HUVECs) stimulated by the two recombinant E2 proteins. The E2-induced apoptosis of HUVECs was confirmed using the molecular marker PARP. The apoptosis rescue observed when the antioxidant N-acetylcysteine was used suggests that reactive oxygen species are involved in E2-induced apoptosis. We propose that these proteins are involved in the chronic inflammation caused by HCV.

摘要

丙型肝炎病毒（HCV）编码大约10种不同的结构和非结构蛋白，包括包膜糖蛋白2（E2）。HCV蛋白，尤其是包膜蛋白，可与细胞受体结合并能损伤组织。内皮炎症是纤维化进展以及肝硬化的最重要决定因素。本研究的目的是评估和比较内皮细胞对在不同表达系统（大肠杆菌和毕赤酵母）中产生的两种重组形式HCV E2蛋白的炎症反应。我们观察到在两种重组E2蛋白刺激下，人脐静脉内皮细胞（HUVECs）出现细胞死亡诱导以及一氧化氮、过氧化氢、白细胞介素-8和血管内皮生长因子A的产生。使用分子标志物PARP证实了E2诱导的HUVECs凋亡。当使用抗氧化剂N-乙酰半胱氨酸时观察到的凋亡挽救表明活性氧参与了E2诱导的凋亡。我们提出这些蛋白参与了由HCV引起的慢性炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/9f9bf3c6cb17/0074-0276-mioc-109-6-0748-gf08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/0c391ac39266/0074-0276-mioc-109-6-0748-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/dd00758f051a/0074-0276-mioc-109-6-0748-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/5e013e5da245/0074-0276-mioc-109-6-0748-gf03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/7f668cdfa233/0074-0276-mioc-109-6-0748-gf04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/eaf808731f24/0074-0276-mioc-109-6-0748-gf05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/a45f04077603/0074-0276-mioc-109-6-0748-gf06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/a63952aa8564/0074-0276-mioc-109-6-0748-gf07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/9f9bf3c6cb17/0074-0276-mioc-109-6-0748-gf08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/0c391ac39266/0074-0276-mioc-109-6-0748-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/dd00758f051a/0074-0276-mioc-109-6-0748-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/5e013e5da245/0074-0276-mioc-109-6-0748-gf03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/7f668cdfa233/0074-0276-mioc-109-6-0748-gf04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/eaf808731f24/0074-0276-mioc-109-6-0748-gf05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/a45f04077603/0074-0276-mioc-109-6-0748-gf06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/a63952aa8564/0074-0276-mioc-109-6-0748-gf07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9631/4238766/9f9bf3c6cb17/0074-0276-mioc-109-6-0748-gf08.jpg

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