Insights into the regulation of chemokine receptors by molecular signaling pathways: Functional roles in neuropathic pain

Fletcher White, Richard J. Miller

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Inflammation plays a central role in the manner that the nervous system responds to injury. These effects include vasodilatation, increased vascular permeability, plasma extravasation, cell migration, and pain. Extracellular signals associated with inflammation may also lead to increased levels of pro-nociceptive chemokines/receptors that directly contribute to persistent or chronic pain behavior. To date, research focused on improving the treatment of chronic pain has largely ignored the role of inflammation-associated transcription factors such as nuclear transcription factor in activated T cells (NFAT). Herein we discuss the idea that activation of this transcription factor may be responsible for the production of chemokines receptors in both neuronal and non-neuronal cells of the peripheral nervous system. Taken together, a better understanding of the transcription of these pro-nociceptive genes may lead to the development of novel analgesic targets.

Original languageEnglish
Pages (from-to)859-865
Number of pages7
JournalBrain, Behavior, and Immunity
Volume24
Issue number6
DOIs
StatePublished - Aug 2010

Fingerprint

Chemokine Receptors
Neuralgia
Transcription Factors
Inflammation
Chronic Pain
Peripheral Nervous System
Capillary Permeability
Plasma Cells
Vasodilation
Nervous System
Cell Movement
Analgesics
T-Lymphocytes
Pain
Wounds and Injuries
Research
Genes
Therapeutics

Keywords

  • CCL2
  • Chemokine
  • CXCL12
  • Neuropathic pain
  • NFAT
  • Transcription factor

ASJC Scopus subject areas

  • Immunology
  • Behavioral Neuroscience
  • Endocrine and Autonomic Systems
  • Medicine(all)

Cite this

Insights into the regulation of chemokine receptors by molecular signaling pathways : Functional roles in neuropathic pain. / White, Fletcher; Miller, Richard J.

In: Brain, Behavior, and Immunity, Vol. 24, No. 6, 08.2010, p. 859-865.

Research output: Contribution to journalArticle

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