Extracellular vesicle glucose transporter-1 and glycan features in monocyte-endothelial inflammatory interactions

Nanomedicine. 2022 Jun:42:102515. doi: 10.1016/j.nano.2022.102515. Epub 2022 Jan 22.

Abstract

Monocyte-induced endothelial cell inflammation is associated with multiple pathological conditions, and extracellular vesicles (EVs) are essential nanosized components of intercellular communication. EVs derived from endotoxin-stimulated monocytes were previously shown to carry pro-inflammatory proteins and RNAs. The role of glucose transporter-1 (GLUT-1) and glycan features in monocyte-derived EV-induced endothelial cell inflammation remains largely unexplored. This study demonstrates that EVs derived from endotoxin-stimulated monocytes activate inflammatory pathways in endothelial cells, which are partially attributed to GLUT-1. Alterations in glycan features and increased levels of GLUT-1 were observed in EVs derived from endotoxin-stimulated monocytes. Notably, inhibition of EV-associated GLUT-1, through the use of fasentin, suppressed EV-induced inflammatory cytokines in recipient endothelial cells.

Keywords: Exosome; Extracellular vesicle; Glucose transporter-1; Glycan node analysis; Inflammation.

MeSH terms

  • Endothelial Cells / metabolism
  • Endothelial Cells / pathology
  • Endotoxins / pharmacology
  • Extracellular Vesicles* / metabolism
  • Glucose Transporter Type 1* / metabolism
  • Humans
  • Inflammation* / metabolism
  • Inflammation* / pathology
  • Monocytes* / metabolism
  • Monocytes* / pathology
  • Polysaccharides* / metabolism

Substances

  • Endotoxins
  • Glucose Transporter Type 1
  • Polysaccharides
  • SLC2A1 protein, human