NDRG2 is expressed on enteric glia and altered in conditions of inflammation and oxygen glucose deprivation/reoxygenation

J Mol Histol. 2021 Feb;52(1):101-111. doi: 10.1007/s10735-020-09927-z. Epub 2020 Nov 17.

Abstract

Enteric glial cells are more abundant than neurons in the enteric nervous system. Accumulating evidence has demonstrated that enteric glial cells share many properties with astrocytes and play pivotal roles in intestinal diseases. NDRG2 is specifically expressed in astrocytes and is involved in various diseases in the central nervous system. However, no studies have demonstrated the expression of NDRG2 in enteric glial cells. We performed immunostaining of adult mouse tissue, human colon sections, and primary enteric glial cells and the results showed that NDRG2 was widely expressed in enteric glial cells. Meanwhile, our results showed that NDRG2 was upregulated after treatment with pro-inflammatory cytokines and exposure to oxygen glucose deprivation/reoxygenation, indicating that NDRG2 might be involved in these conditions. Moreover, we determined that NDRG2 translocated to the nucleus after treatment with pro-inflammatory cytokines but not after exposure to oxygen glucose deprivation/reoxygenation. This study is the first to show the expression and distribution of NDRG2 in the enteric glia. Our results indicate that NDRG2 might be involved in the pathogenesis of enteric inflammation and ischemia/reperfusion injury. This study shows that NDRG2 might be a molecular target for enteric nervous system diseases.

Keywords: Enteric glia; Inflammation; NDRG2; Oxygen glucose deprivation/reoxygenation.

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism*
  • Animals
  • Cell Nucleus / metabolism
  • Enteric Nervous System / metabolism*
  • Glucose / deficiency*
  • Humans
  • Inflammation / pathology*
  • Interleukin-1beta / pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neuroglia / drug effects
  • Neuroglia / metabolism*
  • Neurons / drug effects
  • Neurons / metabolism
  • Oxygen / metabolism*
  • Protein Transport / drug effects
  • Tumor Necrosis Factor-alpha / pharmacology
  • Tumor Suppressor Proteins / metabolism*
  • Up-Regulation / drug effects

Substances

  • Adaptor Proteins, Signal Transducing
  • Interleukin-1beta
  • NDRG2 protein, human
  • Ndr2 protein, mouse
  • Tumor Necrosis Factor-alpha
  • Tumor Suppressor Proteins
  • Glucose
  • Oxygen