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Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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Notch signaling dependent monocyte conversion alleviates immune-mediated neuropathies by regulating RBP-J/NR4A1 axis.

Kaixi Ren1, Sanzhong Li2, Shiqian Liang3

  • 1Department of Neurology, Tangdu Hospital, Air Force Medical University, Xi'an, China; State Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Air Force Medical University, Xi'an, China.

Journal of Autoimmunity
|November 10, 2022
PubMed
Summary

Notch signaling modulates monocyte conversion, reducing nerve damage in a Guillain-Barré syndrome model. This finding highlights Notch signaling

Keywords:
Experimental autoimmune neuritisGuillain-Barré syndromeImmune-mediated neuropathiesMonocyte conversionNR4A1Notch signaling

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Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • Monocytes are crucial in immune-mediated neuropathies like Guillain-Barré syndrome (GBS).
  • The developmental mechanisms of monocyte subpopulations during neuropathy are not fully understood.
  • Notch signaling is implicated in monocyte differentiation and function.

Purpose of the Study:

  • To investigate the role of Notch signaling in monocyte development during experimental autoimmune neuritis (EAN), a model for GBS.
  • To elucidate the mechanisms by which Notch signaling influences monocyte phenotypes and their contribution to neuritis.

Main Methods:

  • Utilized a myeloid-specific Notch signaling activation transgenic mouse (NICcA) model.
  • Assessed clinical scores and performed histopathological examinations of sciatic nerves.
  • Employed flow cytometry, immunofluorescence staining, and RNA sequencing to analyze monocyte populations and gene expression.

Main Results:

  • NICcA EAN mice showed attenuated sciatic nerve injury compared to controls.
  • Increased Ly6Clo monocytes in peripheral blood and nerve tissue correlated with reduced neuritis.
  • Activated Notch signaling promoted a shift towards Ly6Clo monocytes, with Nr4a1 identified as a key mediator.

Conclusions:

  • Monocyte conversion, regulated by Notch signaling, plays a protective role in the EAN mouse model.
  • Targeting Notch signaling and subsequent monocyte differentiation may offer therapeutic strategies for GBS.
  • A link between monocyte conversion and disease severity was observed in human GBS patients.