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Neuropeptide Y induces secretion of high-mobility group box 1 protein in mouse macrophage via PKC/ERK dependent

Jiang-Rui Zhou1, Lu-Ding Zhang, Hua-Feng Wei

  • 1Laboratory of Stress Medicine, Second Military Medical University, No.800 Xiangyin Road, Shanghai 200433, PR China.

Journal of Neuroimmunology
|April 30, 2013
PubMed

Insights

Neuropeptide Y (NPY) directly triggers High Mobility Group Box 1 (HMGB1) release from macrophages, impacting innate immunity. This effect is mediated through Protein Kinase C (PKC) and Extracellular signal-regulated kinase (ERK) pathways.

Area of Science:

  • Immunology
  • Neuroendocrinology
  • Cell Biology

Background:

  • Neuropeptide Y (NPY) is implicated in modulating inflammatory responses.
  • The direct impact of NPY on the release of specific pro-inflammatory mediators remains largely uncharacterized.

Purpose of the Study:

  • To investigate the direct effects of NPY on the release of key pro-inflammatory mediators (TNF-α, IL-1β, IL-6, and HMGB1) from peritoneal macrophages.
  • To elucidate the signaling pathways involved in NPY-induced mediator release.

Main Methods:

  • Primary peritoneal macrophages were treated with NPY.
  • Levels of TNF-α, IL-1β, IL-6, and HMGB1 in the supernatant and cell lysate were measured.
  • The role of Protein Kinase C (PKC) and Extracellular signal-regulated kinase (ERK) pathways was assessed using specific inhibitors.

Main Results:

  • NPY directly induced the release and cytoplasmic translocation of High Mobility Group Box 1 (HMGB1).
  • NPY did not significantly affect the production of Tumor Necrosis Factor-alpha (TNF-α), Interleukin-1 beta (IL-1β), or Interleukin-6 (IL-6).
  • Inhibition of PKC and ERK pathways abrogated the NPY-promoted HMGB1 secretion.

Conclusions:

  • NPY directly potentiates HMGB1 release from macrophages, suggesting a novel role in innate immune system modulation.
  • The findings highlight NPY as a potential regulator of inflammation through HMGB1 signaling.

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