Tanshinone II A Inhibits Tat‐Induced HIV‐1 Transactivation Through Redox‐Regulated AMPK/Nampt Pathway
Identifieur interne : 000F80 ( Main/Exploration ); précédent : 000F79; suivant : 000F81Tanshinone II A Inhibits Tat‐Induced HIV‐1 Transactivation Through Redox‐Regulated AMPK/Nampt Pathway
Auteurs : Hong-Sheng Zhang [République populaire de Chine] ; Xin-Yu Chen [République populaire de Chine] ; Tong-Chao Wu [République populaire de Chine] ; Feng-Juan Zhang [République populaire de Chine]Source :
- Journal of Cellular Physiology [ 0021-9541 ] ; 2014-09.
Abstract
Tat transactivating activity regulated by NAD+‐dependent histone deacetylase sirtuin1 (SIRT1) connects HIV transcription with the metabolic state of the cell. Nicotinamide phosphoribosyltransferase (Nampt) is a rate‐limiting enzyme in the mammalian NAD+ biosynthesis. Nampt, SIRT1, and AMPK were involved in inhibiting HIV‐1 transactivation through redox‐regulated pathway. Tanshinone II A is a main lipid‐soluble monomer derivative from the root of Salvia miltiorrhiza (Danshen) and tanshinone II A possess a variety of biological activities through redox signaling pathway. Here we investigated the effect of tanshinone II A on Tat‐induced HIV‐1 transactivation and the redox signaling pathway involved in it. As the results were shown, tanshinone II A reversed Tat‐induced reactive oxygen species (ROS) production and down‐regulation of glutathione (GSH) levels in TZM‐bl cells through up‐regulation of Nrf2 expression. Tanshinone II A reversed Tat‐induced inhibition of SIRT1 activity but not SIRT1 protein expression. Tanshinone II A reversed Tat‐induced inhibition of Nampt protein expression and depletion of NAD+ levels in TZM‐bl cells in a dose‐dependent manner. Tanshinone II A‐evoked Nampt expression was mediated by AMPK signaling pathway. Tanshinone II A inhibited Tat‐induced HIV‐1 LTR transactivation dependent on AMPK‐Nampt pathway. Collectively, our data provide new insights into understanding of the molecular mechanisms of tanshinone II A inhibited Tat‐regulated transcription, suggesting that targeting AMPK/Nampt/SIRT1 pathway could serve as new anti‐HIV‐1 agents. J. Cell. Physiol. 229: 1193–1201, 2014. © 2014 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/jcp.24552
Affiliations:
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Nicotinamide phosphoribosyltransferase (Nampt) is a rate‐limiting enzyme in the mammalian NAD+ biosynthesis. Nampt, SIRT1, and AMPK were involved in inhibiting HIV‐1 transactivation through redox‐regulated pathway. Tanshinone II A is a main lipid‐soluble monomer derivative from the root of Salvia miltiorrhiza (Danshen) and tanshinone II A possess a variety of biological activities through redox signaling pathway. Here we investigated the effect of tanshinone II A on Tat‐induced HIV‐1 transactivation and the redox signaling pathway involved in it. As the results were shown, tanshinone II A reversed Tat‐induced reactive oxygen species (ROS) production and down‐regulation of glutathione (GSH) levels in TZM‐bl cells through up‐regulation of Nrf2 expression. Tanshinone II A reversed Tat‐induced inhibition of SIRT1 activity but not SIRT1 protein expression. Tanshinone II A reversed Tat‐induced inhibition of Nampt protein expression and depletion of NAD+ levels in TZM‐bl cells in a dose‐dependent manner. Tanshinone II A‐evoked Nampt expression was mediated by AMPK signaling pathway. Tanshinone II A inhibited Tat‐induced HIV‐1 LTR transactivation dependent on AMPK‐Nampt pathway. Collectively, our data provide new insights into understanding of the molecular mechanisms of tanshinone II A inhibited Tat‐regulated transcription, suggesting that targeting AMPK/Nampt/SIRT1 pathway could serve as new anti‐HIV‐1 agents. J. Cell. Physiol. 229: 1193–1201, 2014. © 2014 Wiley Periodicals, Inc.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Zhang, Hong Heng" sort="Zhang, Hong Heng" uniqKey="Zhang H" first="Hong-Sheng" last="Zhang">Hong-Sheng Zhang</name></noRegion><name sortKey="Chen, Xin U" sort="Chen, Xin U" uniqKey="Chen X" first="Xin-Yu" last="Chen">Xin-Yu Chen</name><name sortKey="Wu, Tong Hao" sort="Wu, Tong Hao" uniqKey="Wu T" first="Tong-Chao" last="Wu">Tong-Chao Wu</name><name sortKey="Zhang, Feng Uan" sort="Zhang, Feng Uan" uniqKey="Zhang F" first="Feng-Juan" last="Zhang">Feng-Juan Zhang</name><name sortKey="Zhang, Hong Heng" sort="Zhang, Hong Heng" uniqKey="Zhang H" first="Hong-Sheng" last="Zhang">Hong-Sheng Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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