ArticlePolymers2020
Polyethylene Glycol 35 (PEG35) Modulates Exosomal Uptake and Function.
Article in Polymers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- STATs Signaling Pathways in Acute Pancreatitis: Mechanisms and Regulation.International journal of medical sciences · 2026Review
- Advances in the Functionalization of Vaccine Delivery Systems: Innovative Strategies and Translational Perspectives.Pharmaceutics · 2025Review
- Macrophage-targeted PEGylated liposomes ameliorate experimental autoimmune encephalomyelitis.Frontiers in immunology · 2025Article
- Exosome may be the next generation of promising cell-free vaccines.Human vaccines & immunotherapeutics · 2024Review
- Methods, Mechanisms, and Application Prospects for Enhancing Extracellular Vesicle Uptake.Current medical science · 2024Review
- Exosome engineering in cell therapy and drug delivery.Inflammopharmacology · 2023Review
- Combined Therapy with Simvastatin- and Coenzyme-Q10-Loaded Nanoparticles Upregulates the Akt-eNOS Pathway in Experimental Metabolic Syndrome.International journal of molecular sciences · 2022Article
- Comparison of two isolation methods of tobacco-derived extracellular vesicles, their characterization and uptake by plant and rat cells.Scientific reports · 2022Article
- Comparative Investigation of Cellular Effects of Polyethylene Glycol (PEG) Derivatives.Polymers · 2022Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polyethylene glycols (PEGs) are neutral polymers widely used in biomedical applications due to its hydrophilicity and biocompatibility. Exosomes are small vesicles secreted by nearly all cell types and play an important role in normal and pathological conditions. The purpose of this study was to evaluate the role of a 35-kDa molecular weight PEG (PEG35) on the modulation of exosome-mediated inflammation. Human macrophage-like cells THP-1, epithelial BICR-18, and CAPAN-2 cells were exposed to PEG35 prior to incubation with exosomes of different cellular origins. Exosome internalization was evaluated by confocal microscopy and flow cytometry. In another set of experiments, macrophages were treated with increasing concentrations of PEG35 prior to exposure with the appropriate stimuli: lipopolysaccharide, BICR-18-derived exosomes, or exosomes from acute pancreatitis-induced rats. Nuclear Factor Kappa B (NFκB) and Signal transducer and activator of transcription 3 (STAT3) activation and the expression levels of pro-inflammatory Interleukin 1β (IL1β) were determined. PEG35 administration significantly enhanced the internalization of exosomes in both macrophages and epithelial cells. Further, PEG35 ameliorated the inflammatory response induced by acute pancreatitis-derived exosomes by reducing the expression of IL1β and p65 nuclear translocation. Our results revealed that PEG35 promotes the cellular uptake of exosomes and modulates the pro-inflammatory effect of acute pancreatitis-derived vesicles through inhibition of NFκB, thus emphasizing the potential value of PEG35 as an anti-inflammatory agent for biomedical purposes.
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