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Quinone compounds regulate the level of ROS production by the NADPH oxidase Nox4. | LitMetric

AI Article Synopsis

  • * The study challenges this view by showing that specific quinone derivatives can stimulate Nox4 activity in various cell models, indicating a specific interaction with Nox4 rather than Nox2.
  • * The findings suggest that NQO1 may play a role in this stimulation and highlight how reducing agents can influence Nox4 activity, potentially leading to new treatment targets for diseases involving quinones and Nox4.

Article Abstract

NADPH oxidase Nox4 is expressed in a wide range of tissues and plays a role in cellular signaling by providing reactive oxygen species (ROS) as intracellular messengers. Nox4 oxidase activity is thought to be constitutive and regulated at the transcriptional level; however, we challenge this point of view and suggest that specific quinone derivatives could modulate this activity. In fact, we demonstrated a significant stimulation of Nox4 activity by 4 quinone derivatives (AA-861, tBuBHQ, tBuBQ, and duroquinone) observed in 3 different cellular models, HEK293E, T-REx™, and chondrocyte cell lines. Our results indicate that the effect is specific toward Nox4 versus Nox2. Furthermore, we showed that NAD(P)H:quinone oxidoreductase (NQO1) may participate in this stimulation. Interestingly, Nox4 activity is also stimulated by reducing agents that possibly act by reducing the disulfide bridge (Cys226, Cys270) located in the extracellular E-loop of Nox4. Such model of Nox4 activity regulation could provide new insight into the understanding of the molecular mechanism of the electron transfer through the enzyme, i.e., its potential redox regulation, and could also define new therapeutic targets in diseases in which quinones and Nox4 are implicated.

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Source
http://dx.doi.org/10.1016/j.bcp.2013.03.023DOI Listing

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