TY - JOUR
T1 - Extracellular vesicle glucose transporter-1 and glycan features in monocyte-endothelial inflammatory interactions
AU - Yang, Man
AU - Walker, Sierra A.
AU - Aguilar Díaz de león, Jesús S.
AU - Davidovich, Irina
AU - Broad, Kelly
AU - Talmon, Yeshayahu
AU - Borges, Chad R.
AU - Wolfram, Joy
N1 - Publisher Copyright:
© 2022
PY - 2022/6
Y1 - 2022/6
N2 - 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.
AB - 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.
KW - Exosome
KW - Extracellular vesicle
KW - Glucose transporter-1
KW - Glycan node analysis
KW - Inflammation
UR - http://www.scopus.com/inward/record.url?scp=85126902551&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85126902551&partnerID=8YFLogxK
U2 - 10.1016/j.nano.2022.102515
DO - 10.1016/j.nano.2022.102515
M3 - Article
C2 - 35074500
AN - SCOPUS:85126902551
SN - 1549-9634
VL - 42
JO - Nanomedicine: Nanotechnology, Biology, and Medicine
JF - Nanomedicine: Nanotechnology, Biology, and Medicine
M1 - 102515
ER -