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Targeting the Prokineticin System to Control Chronic Pain and Inflammation.

Lucia Negri1, Daniela Maftei1

  • 1Department of Physiology and Pharmacology "Vittorio Erspamer", Faculty of Medicine, Sapienza University of Roma, Roma, Italy.

Current Medicinal Chemistry
|July 15, 2017
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Summary
This summary is machine-generated.

The prokineticin system, including prokineticin2, plays a key role in chronic pain by activating receptors involved in inflammation and nerve signaling. Inhibiting this system offers a potential new therapeutic target for pain management.

Keywords:
G-coupled receptorsPROK systemProkineticin systemchemokineschronic paininflammation.

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Area of Science:

  • Biochemistry
  • Neuroscience
  • Immunology

Background:

  • Prokineticins (PK1, PK2) are novel chemokines signaling via G-protein coupled receptors (PKR1, PKR2).
  • These receptors are widely distributed and involved in diverse biological processes like inflammation and pain.
  • PK2 is upregulated in inflamed tissues and contributes to pain signaling.

Purpose of the Study:

  • To investigate the role of the prokineticin system in chronic pain mechanisms.
  • To explore prokineticin2 and its receptors in the context of inflammation and nociception.
  • To evaluate the prokineticin system as a therapeutic target for pain relief.

Main Methods:

  • Analysis of prokineticin2 and prokineticin-receptor2 expression in inflamed tissues, dorsal root ganglia, and spinal cord.
  • Investigation of prokineticin receptor activation of TRPV1 and TRPA1 channels.
  • Assessment of prokineticin2's effects on immune cells and cytokine release.

Main Results:

  • PK2 and PKR2 expression increases in dorsal root ganglia and spinal cord following inflammation or injury.
  • Prokineticin receptors activate TRPV1 and TRPA1, contributing to peripheral sensitization.
  • PK2 signaling in the spinal cord and on immune cells promotes central sensitization and inflammation, maintaining chronic pain.

Conclusions:

  • The prokineticin system is critically involved in both peripheral and central sensitization mechanisms of chronic pain.
  • Prokineticin2 signaling on immune cells contributes to inflammatory pain.
  • Inhibition of the prokineticin system presents a promising therapeutic strategy for chronic pain conditions.