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Deficiency of CD93 exacerbates inflammation-induced activation and migration of BV2 microglia by regulating the

Xin Hong1, Mingjie Xia2, Qinyang Zhang3

  • 1Spine Center, Zhongda Hospital of Southeast University, Nanjing, China.

Neuroscience Letters
|October 21, 2022
PubMed

Insights

CD93 (Cluster of Differentiation 93) is upregulated in microglia after spinal cord injury or LPS stimulation. It inhibits NF-κB activation, reducing microglial inflammation and migration, suggesting CD93 as a therapeutic target.

Area of Science:

  • Neuroimmunology
  • Molecular Biology
  • Cellular Biology

Background:

  • CD93's role in inflammatory responses is known.
  • Its specific mechanism in microglial activation and migration post-spinal cord injury (SCI) is unclear.

Purpose of the Study:

  • To investigate the expression and molecular mechanism of CD93 in microglia during neuroinflammation.
  • To elucidate CD93's role in microglial activation and migration following SCI.

Main Methods:

  • Western blot, qRT-PCR, immunofluorescence, Transwell assay, and ELISA were employed.
  • Expression changes and molecular interactions of CD93 in microglia were analyzed post-inflammatory stimuli.

Main Results:

  • CD93 expression increased in microglia after SCI in vivo and lipopolysaccharide (LPS) stimulation in vitro.
  • CD93 was found to interact with TAK1, inhibiting NF-κB activation.
  • This interaction attenuated microglial inflammation and migration.

Conclusions:

  • CD93 plays a role in microglia-mediated neuroinflammation post-SCI.
  • CD93 represents a potential therapeutic target for neuroimmunological regulation.
Keywords:
CD93InflammationMicrogliaNF-κBSpinal cord injury

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