Artículos de revistas
Inflammatory response of endothelial cells to hepatitis C virus recombinant envelope glycoprotein 2 protein exposure
Fecha
2014-09-01Registro en:
Memórias do Instituto Oswaldo Cruz. Instituto Oswaldo Cruz, Ministério da Saúde, v. 109, n. 6, p. 748-756, 2014.
0074-0276
10.1590/0074-0276140090
S0074-02762014000600748
S0074-02762014000600748.pdf
4066413997908572
6720223715917381
0000-0002-3350-8308
Autor
Escola de Ciências Farmacêuticas Departamento de Análises Clínicas Laboratório de Imunologia Clínica
Universidade Estadual Paulista (Unesp)
Universidade Nova de Lisboa Instituto de Higiene e Medicina Tropcal Departamento de Parasitologia Médica
Universidade Federal de São Carlos (UFSCar)
Universidade Federal de São Carlos (UFSCar)
Universidade de São Paulo (USP)
Institución
Resumen
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.