Rab27a Contributes to the Processing of Inflammatory Pain in Mice

Cells. 2020 Jun 18;9(6):1488. doi: 10.3390/cells9061488.

Abstract

Tissue injury and inflammation may result in chronic pain, a severe debilitating disease that is associated with great impairment of quality of life. An increasing body of evidence indicates that members of the Rab family of small GTPases contribute to pain processing; however, their specific functions remain poorly understood. Here, we found using immunofluorescence staining and in situ hybridization that the small GTPase Rab27a is highly expressed in sensory neurons and in the superficial dorsal horn of the spinal cord of mice. Rab27a mutant mice, which carry a single-nucleotide missense mutation of Rab27a leading to the expression of a nonfunctional protein, show reduced mechanical hyperalgesia and spontaneous pain behavior in inflammatory pain models, while their responses to acute noxious mechanical and thermal stimuli is not affected. Our study uncovers a previously unrecognized function of Rab27a in the processing of persistent inflammatory pain in mice.

Keywords: Rab27a; dorsal root ganglia; inflammatory pain; mice; spinal cord.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal
  • Female
  • Ganglia, Spinal / physiopathology
  • Gene Expression
  • Hyperalgesia / physiopathology
  • Immunohistochemistry
  • In Situ Hybridization
  • Inflammation / physiopathology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Mutation, Missense
  • Pain / physiopathology*
  • Pain Measurement
  • Sensory Receptor Cells / physiology
  • Spinal Cord / physiopathology
  • rab27 GTP-Binding Proteins / deficiency
  • rab27 GTP-Binding Proteins / genetics
  • rab27 GTP-Binding Proteins / physiology*

Substances

  • rab27 GTP-Binding Proteins
  • Rab27a protein, mouse