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TRAF6-p38/JNK-ATF2 axis promotes microglial inflammatory activation.

Mengmeng Li1, Dongmei Zhang2, Xin Ge1

  • 1Clinical Medicine Research Center, Affiliated Hospital 2 of Nantong University, Nantong 226001, People's Republic of China; Jiangsu Key Laboratory of Neurogeneration, Nantong University, Nantong 226001, People's Republic of China.

Experimental Cell Research
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PubMed
Summary

Activating transcription factor 2 (ATF2) promotes neuroinflammation by activating microglia. Inhibiting this pathway may offer a new therapeutic target for central nervous system (CNS) diseases.

Keywords:
ATF2JNK/p38 signaling pathwayMicrogliaNeuroinflammationTRAF6

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Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Activating transcription factor 2 (ATF2) is involved in inflammatory responses but its role in the central nervous system (CNS) is unclear.
  • Neuroinflammation is implicated in various CNS diseases.

Purpose of the Study:

  • To investigate the expression and biological function of ATF2 in CNS inflammation.
  • To elucidate the molecular mechanisms underlying ATF2's role in microglia activation.

Main Methods:

  • Used a lipopolysaccharide (LPS)-induced neuroinflammation mouse model.
  • Investigated ATF2 expression, phosphorylation, and localization in microglia (BV2 cells) in vitro.
  • Utilized ATF2 inhibition, TRAF6 knockdown, and specific pathway inhibitors (p38, JNK).

Main Results:

  • ATF2 was upregulated and co-localized with microglia in inflamed mouse brains.
  • LPS treatment increased ATF2 expression, phosphorylation, and nuclear accumulation in microglia.
  • ATF2 inhibition reduced pro-inflammatory factors and neuronal apoptosis.
  • TRAF6 knockdown suppressed LPS-induced ATF2 activation via the JNK/p38 pathway.

Conclusions:

  • ATF2 plays a pro-inflammatory role in microglia.
  • The TRAF6-JNK/p38-ATF2 axis promotes microglial activation and neuronal injury in CNS inflammation.
  • This axis represents a potential therapeutic target for CNS diseases.