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Nitric oxide upregulates microglia phagocytosis and increases transient receptor potential vanilloid type 2 channel

Matthew J E Maksoud1,2, Vasiliki Tellios1,2, Dong An2

  • 1Graduate Program of Neuroscience, The University of Western Ontario, London, Canada.

Glia
|August 28, 2019
PubMed

Insights

Nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) enhances microglial phagocytosis by increasing TRPV2 channel activity and plasma membrane expression. This pathway is crucial for central nervous system health.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglial phagocytosis is vital for CNS development and function.
  • Dysregulated phagocytosis is linked to neurological disorders.
  • Initial phagocytosis involves nitric oxide (NO) and TRPV2 channels in microglia.

Purpose of the Study:

  • To investigate the regulatory role of inducible nitric oxide synthase (iNOS)/NO signaling in microglial phagocytosis.
  • To determine the effect of iNOS/NO on transient receptor potential vanilloid type 2 (TRPV2) channel activation.
  • To elucidate the signaling pathways involved in NO-mediated regulation of phagocytosis and TRPV2 activity.

Main Methods:

  • Phagocytosis assays
  • Calcium imaging
  • Patch clamp electrophysiology
  • Immunocytochemistry
  • Immunoblot assays
  • Use of iNOS-knockout (iNOS-/-) mice and wild-type (WT) controls
  • Application of NO-donors and specific inhibitors (PKG, PI3K)

Main Results:

  • iNOS-/- microglia showed significantly reduced phagocytic capacity and TRPV2 channel activity compared to WT.
  • TRPV2 protein levels on the plasma membrane were lower in iNOS-/- microglia, without changes in mRNA.
  • NO-donor treatment restored phagocytosis and TRPV2 activity in iNOS-/- microglia.
  • Inhibition of iNOS, PKG, or PI3K decreased TRPV2 activity and plasma membrane expression in WT microglia.

Conclusions:

  • iNOS/NO signaling is essential for optimal microglial phagocytosis.
  • iNOS/NO signaling upregulates microglial phagocytosis by promoting TRPV2 trafficking to the plasma membrane.
  • This regulation occurs through a pathway involving PKG and PI3K.
Keywords:
TRPV2calciumnitric oxidephagocytosisprotein kinase G

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