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Nevirapine induced mitochondrial dysfunction in HepG2 cells
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Metadata
Document Title
Nevirapine induced mitochondrial dysfunction in HepG2 cells
Author
Paemanee A., Sornjai W., Kittisenachai S., Sirinonthanawech N., Roytrakul S., Wongtrakul J., Smith D.R.
Name from Authors Collection
Scopus Author ID
55043184800
Affiliations
Institute of Molecular Biosciences, Mahidol University, Bangkok, Thailand; Genome Technology Research Unit, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathumthani, Thailand; Research Institute for Health Sciences, Chiang Mai University, Chiang Mai, Thailand
Type
Article
Source Title
Scientific Reports
ISSN
20452322
Year
2017
Volume
7
Issue
1
Open Access
Gold, Green
Publisher
Nature Publishing Group
DOI
10.1038/s41598-017-09321-y
Abstract
Nevirapine (NVP) is a non-nucleoside reverse transcriptase inhibitor frequently used in combination with other antiretroviral agents for highly active antiretroviral therapy (HAART) of patients infected with the human immunodeficiency virus type 1 (HIV-1). However NVP can cause serious, life-threatening complications. Hepatotoxicity is one of the most severe adverse effects, particularly in HIV patients with chronic hepatitis C virus co-infection as these patients can develop liver toxicity after a relatively short course of treatment. However, the mechanism of NVP-associated hepatotoxicity remains unclear. This study sought to investigate the effect of NVP on protein expression in liver cells using a proteomic approach. HepG2 cells were treated or not treated with NVP and proteins were subsequently resolved by two-dimensional gel electrophoresis. A total of 33 differentially regulated proteins were identified, of which nearly 40% (13/33) were mitochondrial proteins. While no obvious differences were observed between NVP treated and untreated cells after staining mitochondria with mitotracker, RT-PCR expression analysis of three mitochondrially encoded genes showed all were significantly up-regulated in NVP treated cells. Mitochondrial dysfunction was observed in response to treatment even with slightly sub-optimal therapeutic treatment concentrations of NVP. This study shows that NVP induces mitochondrial dysregulation in HepG2 cells. © 2017 The Author(s).
Industrial Classification
Knowledge Taxonomy Level 1
Knowledge Taxonomy Level 2
Knowledge Taxonomy Level 3
Funding Sponsor
Mahidol University; Thailand Research Fund; National Research Council of Thailand
License
CC BY
Rights
Author
Publication Source
Scopus