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NFAT1 Signaling Contributes to Bone Cancer Pain by Regulating IL-18 Expression in Spinal Microglia.

Xuetai Chen1, Ying Zeng1, Zizhu Wang2

  • 1Jiangsu Province Key Laboratory of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application Technology, NMPA Key Laboratory for Research and Evaluation of Narcotic and Psychotropic Drugs, Department of Anesthesiology, The Yancheng Clinical College of Xuzhou Medical University, The First people's Hospital of Yancheng, Yancheng, China.

CNS Neuroscience & Therapeutics
|February 17, 2025
PubMed
Summary
This summary is machine-generated.

Nuclear factor of activated T cells 1 (NFAT1) signaling in spinal microglia drives bone cancer pain by increasing interleukin-18 (IL-18). Inhibiting NFAT1 alleviates pain behaviors, suggesting NFAT1 as a therapeutic target.

Keywords:
bone cancer paininterleukin‐18microglianuclear factor of activated T cells 1p38 MAPK

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Area of Science:

  • Neuroscience
  • Immunology
  • Oncology

Background:

  • Bone cancer pain involves complex mechanisms including neuroinflammation.
  • Spinal microglia play a crucial role in pain sensitization.

Purpose of the Study:

  • To investigate the role of nuclear factor of activated T cells 1 (NFAT1) signaling in spinal microglia in bone cancer pain.
  • To determine if NFAT1 regulates interleukin-18 (IL-18) expression in the context of bone cancer pain.

Main Methods:

  • A mouse model of Lewis lung carcinoma-induced bone cancer pain was utilized.
  • Nociceptive behaviors (mechanical allodynia, thermal hyperalgesia, spontaneous pain) were assessed.
  • NFAT1 and IL-18 expression, p38 MAPK phosphorylation, and neuronal/microglial activation were analyzed using molecular and imaging techniques.

Main Results:

  • NFAT1 expression was significantly upregulated in spinal microglia following tumor inoculation.
  • Pharmacological inhibition of NFAT1 reversed and prevented bone cancer pain behaviors.
  • NFAT1 inhibition reduced p38 MAPK phosphorylation and IL-18 production, suppressed microglial activation, and attenuated N-methyl-D-aspartate receptor signaling.

Conclusions:

  • Spinal microglia NFAT1-p38 signaling contributes to bone cancer pain via IL-18-mediated central sensitization.
  • NFAT1 represents a promising therapeutic target for managing bone cancer pain.