Respiratory syncytial virus infection down-regulates antioxidant enzyme expression by triggering deacetylation-proteasomal degradation of Nrf2
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- 作者：Narayana Komaravellia ; Bing Tianb ; Teodora Ivanciuca ; Nicholas Mautempsa ; Allan R. Brasierb ; c ; Roberto P. Garofaloa ; Antonella Casolaa ; c ; ancasola@utmb.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：AEC ; Airway epithelial cell ; AOE ; Antioxidant enzyme ; ARE ; Antioxidant response element ; BHA ; Butylated hydroxyanisole ; ChIP ; Chromatin immunoprecipitation ; GCLC ; Glutamyl cysteine ligase-catalytic ; GPX1 ; Glutathione peroxidase 1 ; HDAC ; Histone deacetylase ; IP ; Immunoprecipitation ; Keap1 ; Kelch-like-ECH-associated protein 1 ; NQO1 ; NAD(P)H ; quinone oxidoreductase 1 ; Nrf2 ; Nuclear factor erythroid 2-related factor 2 ; QgPCR ; Quantitative genomic PCR ; ROS ; Reactive oxygen species ; RSV ; Respiratory sy
- 刊名：Free Radical Biology and Medicine
- 出版年：2015
- 出版时间：November 2015
- 年：2015
- 卷：88
- 期：part_PB
- 页码：391-403
- 全文大小：2892 K
文摘
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RSV infection in vitro and in vivo causes oxidative damage by reducing Nrf2-dependent gene transcription of antioxidant enzymes.
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RSV induces Nrf2 deacetylation, ubiquitination, and proteasomal degradation in vitro and in vivo.
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Histone deacetylase and proteasome inhibitors block Nrf2 degradation and restore Nrf2-dependent gene expression.
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Nrf2 inducers restore Nrf2 -dependent gene expression in the context of RSV infection in vitro and in vivo.