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Macrophage achieves self-protection against oxidative stress-induced ageing through the Mst-Nrf2 axis

Ping Wang1,2, Jing Geng1,2, Jiahui Gao1

  • 1State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361102, China.

Nature Communications
|February 16, 2019
PubMed

Insights

Kinases Mst1 and Mst2 (Mst1/2) sense reactive oxygen species (ROS) and protect cells from oxidative stress by stabilizing the antioxidant factor Nrf2. This Mst-Nrf2 pathway is crucial for cellular defense and survival during antimicrobial responses.

Area of Science:

  • Cellular Biology
  • Immunology
  • Biochemistry

Background:

  • Phagocytes produce reactive oxygen species (ROS) to fight pathogens, but cellular protection against this oxidative stress is not fully understood.
  • Oxidative stress can damage cells, highlighting the need for self-protective mechanisms.

Purpose of the Study:

  • To elucidate the cellular mechanism that protects against oxidative damage during antimicrobial responses.
  • To identify the role of kinases Mst1 and Mst2 (Mst1/2) in sensing ROS and maintaining redox balance.

Main Methods:

  • Investigated the interaction of Mst1/2 with cellular membranes (phagosomal, mitochondrial) upon ROS release.
  • Examined the phosphorylation of kelch like ECH associated protein 1 (Keap1) by Mst1/2.
  • Assessed the effect of N-acetylcysteine on the Mst1/2-Keap1-Nrf2 pathway.
  • Studied the consequences of Mst1/2 loss on oxidative injury and phagocyte viability.

Main Results:

  • Mst1/2 kinases are recruited to membranes by ROS and activated to phosphorylate Keap1, preventing Nrf2 degradation.
  • This Mst1/2-mediated stabilization of Nrf2 protects cells from oxidative damage.
  • Antioxidant treatment disrupts Mst1/2 membrane association and signaling.
  • Loss of Mst1/2 leads to increased oxidative injury, phagocyte aging, and death.

Conclusions:

  • The Mst1/2-Nrf2 axis acts as a critical ROS-sensing and antioxidant mechanism.
  • This pathway is essential for cellular protection and survival during antimicrobial responses.

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