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Autophagy regulates MAVS signaling activation in a phosphorylation-dependent manner in microglia

Jinbo Cheng1, Yajin Liao1,2, Lei Xiao1

  • 1The State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.

Cell Death and Differentiation
|February 1, 2017
PubMed

Insights

Mitochondrial antiviral signaling (MAVS) pathway regulates brain inflammation and is controlled by autophagy. Targeting MAVS may treat neuroinflammatory diseases.

Area of Science:

  • Neuroimmunology
  • Molecular Biology
  • Cellular Signaling

Background:

  • Mitochondrial antiviral signaling (MAVS) protein is crucial for antiviral immunity and autoimmunity.
  • The specific role of MAVS signaling in the brain remains largely unknown.

Purpose of the Study:

  • To investigate the presence and function of MAVS signaling in the brain.
  • To elucidate the regulatory mechanisms of MAVS in neuroinflammation.
  • To explore MAVS as a potential therapeutic target for brain diseases.

Main Methods:

  • Poly(I:C) administration to induce inflammation in the brain.
  • Analysis of MAVS and autophagy activation.
  • LC3 binding assays and LIR motif identification.
  • c-Abl kinase phosphorylation studies.
  • MPTP-induced neurodegeneration model in vivo.

Main Results:

  • MAVS signaling mediates poly(I:C)-induced brain inflammation.
  • Autophagy activation negatively regulates MAVS via LC3 binding.
  • c-Abl kinase phosphorylates MAVS, influencing LC3 interaction and downstream signaling.
  • MAVS and c-Abl deficiency protect against MPTP-induced microglial activation and dopaminergic neuron loss.

Conclusions:

  • MAVS signaling is present and active in the brain, contributing to neuroinflammation.
  • Autophagy and c-Abl kinase are key regulators of MAVS activity in the nervous system.
  • MAVS-dependent microglial activation is a critical factor in neurodegenerative diseases, offering a potential therapeutic target.

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