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Nuclear Factor-κB Signaling Regulates the Nociceptin Receptor but Not Nociceptin Itself
Lan Zhang1,2, Ulrike M Stamer1,2, Robin Moolan-Vadackumchery1,2,3
1Department of Anaesthesiology and Pain Medicine, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
Cells
|January 8, 2025
Summary
The nociceptin system, involving the nociceptin receptor (NOP) and nociceptin, may have an anti-inflammatory role. Nuclear factor-κB (NFκB) signaling regulates NOP transcription, influencing inflammatory responses.
Area of Science:
- Immunology and Molecular Biology
- Neuroscience and Pain Research
Background:
- The nociceptin receptor (NOP) and its ligand nociceptin are implicated in pain and inflammation pathways.
- Nuclear factor-κB (NFκB) is a key regulator of inflammatory processes, including the production of cytokines like TNF-α and IL-1β.
Purpose of the Study:
- To investigate the role of NFκB signaling in modulating the nociceptin system under inflammatory conditions.
- To examine the impact of tumor necrosis factor-α (TNF-α) and interleukin (IL)-1β on NOP and prepronociceptin (ppNOC) expression in human THP-1 cells.
Main Methods:
- Human THP-1 cells were stimulated with phorbol-myristate-acetate (PMA) and/or inflammatory cytokines (TNF-α, IL-1β).
- NFκB signaling was inhibited using BAY 11-7082, JSH-23, or anacardic acid.
- Gene expression (NOP, ppNOC mRNA) was quantified via RT-qPCR, and protein levels were assessed by flow cytometry and ImageStream analysis.
Main Results:
- Proinflammatory cytokines (TNF-α, IL-1β) suppressed NOP and ppNOC mRNA levels in PMA-stimulated cells.
- NFκB inhibitors (BAY 11-7082, JSH-23) reversed the TNF-α-induced repression of NOP mRNA.
- TNF-α significantly promoted NFκB/p65 nuclear translocation, while IL-1β did not.
Conclusions:
- NFκB signaling is a critical regulator of NOP transcription in the context of inflammation.
- The nociceptin system may exert anti-inflammatory effects during immune responses, potentially through NFκB-mediated regulation.
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