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

doi:10.1016/j.nano.2022.102515

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

Houston Methodist

Research output: Contribution to journal › Article › peer-review

26 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 language	English (US)
Article number	102515
Pages (from-to)	102515
Journal	Nanomedicine: Nanotechnology, Biology, and Medicine
Volume	42
DOIs	https://doi.org/10.1016/j.nano.2022.102515
State	Published - 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
General Materials Science
Biomedical Engineering
Medicine (miscellaneous)
Pharmaceutical Science

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10.1016/j.nano.2022.102515

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Yang, M., Walker, S. A., Aguilar Díaz de león, J. S., Davidovich, I., Broad, K., Talmon, Y., Borges, C. R., & Wolfram, J. (2022). Extracellular vesicle glucose transporter-1 and glycan features in monocyte-endothelial inflammatory interactions. Nanomedicine: Nanotechnology, Biology, and Medicine, 42, 102515. Article 102515. https://doi.org/10.1016/j.nano.2022.102515

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title = "Extracellular vesicle glucose transporter-1 and glycan features in monocyte-endothelial inflammatory interactions",

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, Endotoxins/pharmacology, Humans, Inflammation/metabolism, Polysaccharides/metabolism, Extracellular Vesicles/metabolism, Endothelial Cells/metabolism, Glucose Transporter Type 1/metabolism, Monocytes/metabolism",

author = "Man Yang and Walker, \{Sierra A.\} and \{Aguilar D{\'i}az de le{\'o}n\}, \{Jes{\'u}s S.\} and Irina Davidovich and Kelly Broad and Yeshayahu Talmon and Borges, \{Chad R.\} and Joy Wolfram",

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month = jun,

doi = "10.1016/j.nano.2022.102515",

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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

PY - 2022/6

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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

KW - Endotoxins/pharmacology

KW - Humans

KW - Inflammation/metabolism

KW - Polysaccharides/metabolism

KW - Extracellular Vesicles/metabolism

KW - Endothelial Cells/metabolism

KW - Glucose Transporter Type 1/metabolism

KW - Monocytes/metabolism

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

Abstract

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