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

Man Yang, Sierra A. Walker, Jesús S. Aguilar Díaz de león, Irina Davidovich, Kelly Broad, Yeshayahu Talmon, Chad R. Borges, Joy Wolfram

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

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.

Original languageEnglish (US)
Article number102515
Pages (from-to)102515
JournalNanomedicine: Nanotechnology, Biology, and Medicine
Volume42
DOIs
StatePublished - Jun 2022

Keywords

  • Exosome
  • Extracellular vesicle
  • Glucose transporter-1
  • Glycan node analysis
  • Inflammation
  • Endotoxins/pharmacology
  • Humans
  • Inflammation/metabolism
  • Polysaccharides/metabolism
  • Extracellular Vesicles/metabolism
  • Endothelial Cells/metabolism
  • Glucose Transporter Type 1/metabolism
  • Monocytes/metabolism

ASJC Scopus subject areas

  • Bioengineering
  • Molecular Medicine
  • Materials Science(all)
  • Biomedical Engineering
  • Medicine (miscellaneous)
  • Pharmaceutical Science

Fingerprint

Dive into the research topics of 'Extracellular vesicle glucose transporter-1 and glycan features in monocyte-endothelial inflammatory interactions'. Together they form a unique fingerprint.

Cite this