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 - Funding Information:
This work is partially supported by the Mayo Clinic Florida Center for Regenerative Medicine (JW), the Mayo Clinic Center for Biomedical Discovery (JW), and the China Scholarship Council (MY). The cryo-TEM work was performed at the Technion Center for Electron Microscopy of Soft Matter. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funding agencies. The graphical abstract and Figure 5 , A were made in ©BioRender - biorender.com .
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
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U2 - 10.1016/j.nano.2022.102515
DO - 10.1016/j.nano.2022.102515
M3 - Article
C2 - 35074500
AN - SCOPUS:85126902551
VL - 42
JO - Nanomedicine: Nanotechnology, Biology, and Medicine
JF - Nanomedicine: Nanotechnology, Biology, and Medicine
SN - 1549-9634
M1 - 102515
ER -