Nikhil Prasad Fact checked by:Thailand Medical News Team Sep 12, 2026 49 minutes ago
High blood sugar may damage blood vessels not only through its direct effects on cells, but also by changing the microscopic packages cells use to communicate with each other. New laboratory findings suggest prolonged exposure to high glucose alters extracellular vesicles (EVs), giving some of these cellular messengers properties that could intensify vascular inflammation.
High glucose may transform extracellular vesicles into cellular messengers that promote vascular inflammation and monocyte
adhesion
The research, detailed in this
Thailand Medical News report, provides evidence that hyperglycemia changes EV protein cargo and can make monocytes more likely to attach to endothelial cells, an important process in inflammatory vascular disease.
The study involved scientists from Fundação Oswaldo Cruz (Fiocruz Paraná), Instituto Carlos Chagas, Laboratório de Pesquisa em Apicomplexa, Curitiba, Paraná, Brazil, and the Laboratório de Imunologia Molecular, Celular e Inteligência Artificial at Instituto Carlos Chagas, Fiocruz Paraná, Curitiba, Paraná, Brazil.
High Glucose Switches on Vascular Inflammation
Scientists compared human brain microvascular endothelial cells exposed long-term to normal glucose of 5.5 millimolar (mM), equivalent to approximately 99.9 mg/dL, with cells maintained at 33 mM glucose, approximately 594 mg/dL.
Although high glucose did not significantly affect cell viability, it strongly activated inflammatory signals. ICAM-1 expression increased nearly 1.5-fold, while VCAM-1 messenger RNA jumped 51.8-fold and MCP-1 increased 5.3-fold. IL-8 also increased threefold, although this change was not statistically significant.
These changes matter because molecules including ICAM-1 and VCAM-1 help immune cells attach to the endothelium, while MCP-1 helps recruit monocytes toward sites of inflammation.
High Glucose Reprograms Extracellular Vesicles
The scientists next examined EVs released by endothelial cells and THP-1 monocytes. EVs are membrane-bound particles containing biological cargo that can influence other cells.
High glucose did not substantially change EV size, but endothelial cells exposed to high glucose released approximately four times fewer particles. THP-1 monocytes showed no significant change in EV release.
Protein analysis revealed major differences. Scientists detected 342 proteins in endothelial EVs, with 102 differing between glucose conditions. Thirty-seven proteins were differentially expressed in high-glucose EVs.
The altered cargo pointed toward metabolism, inflammation and endothelial barrier disruption. High-glucose endothelial EVs contained changes involving proteins associated with glycolytic metabolism and proteins including CLIC1, CLIC4, EZR and IQGAP1, which are connected with mechanisms regulating the cytoskeleton, tight junctions and endothelial barrier function.
Immune-Cell EVs Beco
me More Inflammatory
Scientists identified 652 proteins in THP-1 EVs, including 159 that differed between normal- and high-glucose conditions.
High-glucose THP-1 EVs showed enrichment in processes involving inflammation, cytotoxicity, secretion, glucose responses and antigen presentation. Cathepsin G, a serine protease associated with immune activation, was prominent under high-glucose conditions.
EVs Encourage Monocytes to Stick to Endothelial Cells
The most significant functional result emerged when endothelial cells were exposed to EVs before fluorescently labeled monocytes were introduced.
High-glucose EVs increased monocyte adhesion, with EVs from THP-1 cells exposed to 33 mM glucose producing the strongest effect. Control experiments indicated that EVs themselves contributed to the increased adhesion rather than glucose concentration alone.
Conclusions
The findings suggest prolonged high glucose can alter endothelial inflammatory activity while simultaneously changing EV production, protein cargo and biological function. These altered cellular messages could potentially reinforce vascular inflammation and monocyte recruitment during chronic hyperglycemia. However, the experiments involved cultured cell lines and lacked an osmotic control, meaning primary-cell, animal and human studies are needed to establish their relevance to diabetic vascular disease.
The study findings were published in the peer reviewed International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/27/18/8107
Read Also:
https://www.thailandmedical.news/articles/diabetes
Share
Tweet
Share
