Prion protein participates in the regulation of classical and alternative activation of BV2 microglia

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Adipose-Derived Mesenchymal Stromal Cells Co-Cultured with Primary Mixed Glia to Reduce Prion-Induced Inflammation
10:40

Adipose-Derived Mesenchymal Stromal Cells Co-Cultured with Primary Mixed Glia to Reduce Prion-Induced Inflammation

Published on: August 11, 2023

Fushan Shi1, Lifeng Yang, Mohammed Kouadir

  • 1State Key Laboratories for Agrobiotechnology, Key Lab of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing, China.

Journal of Neurochemistry
|October 16, 2012
PubMed

Insights

The cellular prion protein (PrP(C)) regulates microglial activation. Down-regulating its gene (PRNP) impacts responses to inflammatory signals, suggesting a role in neuroinflammation.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Cellular prion protein (PrP(C)) is a cell surface glycoprotein with suggested neuroprotective roles.
  • PrP(C) function is context-dependent, influencing responses to cellular stress.
  • Microglia are key immune cells in the central nervous system, involved in neuroinflammation.

Purpose of the Study:

  • To investigate the effect of down-regulating the prion protein gene (PRNP) on microglial activation.
  • To analyze how PRNP silencing influences microglial responses to specific cytokines (IFN-γ, IL-4, IL-10).

Main Methods:

  • Examined PRNP mRNA expression in BV2 microglia exposed to IFN-γ, IL-4, or IL-10.
  • Utilized siRNA to silence PRNP expression in microglia.
  • Assessed microglial activation parameters following cytokine stimulation in PRNP-silenced cells.

Main Results:

  • PRNP mRNA expression decreased in microglia upon exposure to IFN-γ, IL-4, or IL-10.
  • PRNP silencing reduced microglial responsiveness to IFN-γ.
  • Silencing PRNP significantly altered the phenotype of IL-4-induced microglial activation.
  • PRNP silencing had no significant effect on IL-10-induced microglial activation.

Conclusions:

  • PrP(C) plays a role in modulating the transition of microglia from a quiescent to an activated state.
  • PrP(C) is involved in regulating microglial responses during classical and alternative activation pathways.
  • These findings highlight PrP(C)'s contribution to neuroinflammatory processes.

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