Nrf2: new insight in cell apoptosis.

M Bonay,T B Deramaudt

doi:10.1038/cddis.2015.256

Abstract

Nrf2: new insight in cell apoptosis.

Highlights

In a recent issue of Cell Death and Discovery, we described a new mechanism by which sulforaphane decreased mycobacterial burden in an in vitro model of THP-1-derived macrophage infection by Mycobacterium abscessus.[1]
This sulforaphane-mediated diminution was due to the induction of a caspase-independent cell apoptosis and necessitated activation of both nuclear factor E2-related factor 2 (Nrf2) and p38 mitogen-activated protein kinases (MAPK) signaling pathways
The results showed an inhibition of mycobacterial growth 7 days postinfection in sulforaphane pretreated macrophages compared with vehicle pretreated ones

Summary

Introduction

In a recent issue of Cell Death and Discovery, we described a new mechanism by which sulforaphane decreased mycobacterial burden in an in vitro model of THP-1-derived macrophage infection by Mycobacterium abscessus.[1]. In a recent issue of Cell Death and Discovery, we described a new mechanism by which sulforaphane decreased mycobacterial burden in an in vitro model of THP-1-derived macrophage infection by Mycobacterium abscessus.[1] This sulforaphane-mediated diminution was due to the induction of a caspase-independent cell apoptosis and necessitated activation of both nuclear factor E2-related factor 2 (Nrf2) and p38 mitogen-activated protein kinases (MAPK) signaling pathways. It is unsurprising that the use of oxidant scavengers such as MnTE-2-PyP or N-acetyl-L-cysteine has been shown to decrease M. abscessus load by activating bacterial killing in phagolysosomes.[4] In our study, we decreased the oxidative environment in THP-1-derived macrophages by activating Nrf[2], the key transcription factor that controls the cascade of cytoprotective and antioxidant defense mechanisms, and the maintenance of the redox homeostasis.

Results

Conclusion