Aβ Induces Neuroinflammation and Microglial M1 Polarization via cGAS-STING-IFITM3 Signaling Pathway in BV-2 Cells

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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates

Published on: January 30, 2014

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Zheng Wu1, Wei Tang2, Fatima Elzahra E M Ibrahim1

  • 1Department of Neurology, The Second Hospital of Dalian Medical University, No. 467 Zhongshan Road, Shahekou District, Dalian City, 116023, Liaoning Province, China.

Neurochemical Research
|May 20, 2023
PubMed

Insights

Alzheimer's disease involves microglia-mediated neuroinflammation. This study reveals the cGAS-STING-IFITM3 pathway in microglia contributes to Aβ-induced inflammation, offering potential therapeutic targets.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglia are brain's innate immune cells, crucial for monitoring and responding to the microenvironment.
  • Microglia-driven neuroinflammation is increasingly implicated in Alzheimer's disease (AD) pathogenesis.
  • Understanding molecular mechanisms in microglia is vital for AD research.

Purpose of the Study:

  • To investigate the role of Interferon-induced transmembrane protein 3 (IFITM3) in microglia during Alzheimer's disease.
  • To explore the regulation of IFITM3 by cGAS-STING signaling in activated microglia.
  • To elucidate the involvement of the cGAS-STING-IFITM3 axis in amyloid-beta (Aβ)-induced neuroinflammation.

Main Methods:

  • Investigated IFITM3 expression in microglia treated with Aβ peptides.
  • Performed in vitro knockdown of IFITM3 to assess its effect on microglial polarization.
  • Examined the regulation of IFITM3 by cGAS-STING signaling pathway.

Main Results:

  • IFITM3 expression was significantly upregulated in microglia upon Aβ treatment.
  • Knockdown of IFITM3 suppressed M1-like polarization of microglia.
  • IFITM3 expression in activated microglia is regulated by cGAS-STING signaling.
  • Inhibition of cGAS-STING signaling led to reduced IFITM3 expression.

Conclusions:

  • The cGAS-STING-IFITM3 signaling axis plays a significant role in Aβ-induced neuroinflammation within microglia.
  • IFITM3 is a key mediator in microglial response to Aβ, influencing their inflammatory polarization.
  • Targeting the cGAS-STING-IFITM3 pathway may offer a novel therapeutic strategy for Alzheimer's disease.
Keywords:
Alzheimer's diseaseIFITM3NeuroinflammationcGAS-STING

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