ArticleOpen life sciences2020
Influences of advanced glycosylation end products on the inner blood-retinal barrier in a co-culture cell model
Article in Open life sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Advances in Modeling the Inner Blood-Retinal Barrier: From Static Tissue Cell Cultures to Microphysiological Systems.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Use of physiologically based kinetic modeling to predict neurotoxicity and genotoxicity of methylglyoxal in humans.NPJ science of food · 2024Article
- The mechanics of the retina: Müller glia role on retinal extracellular matrix and modelling.Frontiers in medicine · 2024Review
- Enzyme-activatable kidney-targeted dendrimer-drug conjugate for efficient childhood nephrotic syndrome therapy.Theranostics · 2024Article
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycosylation end products (AGEs) are harmful factors that can damage the inner blood-retinal barrier (iBRB). Rat retinal microvascular endothelial cells (RMECs) were isolated and cultured, and identified by anti-CD31 and von Willebrand factor polyclonal antibodies. Similarly, rat retinal Müller glial cells (RMGCs) were identified by H&E staining and with antibodies of glial fibrillary acidic protein and glutamine synthetase. The transepithelial electrical resistance (TEER) value was measured with a Millicell electrical resistance system to observe the leakage of the barrier. Transwell cell plates for co-culturing RMECs with RMGCs were used to construct an iBRB model, which was then tested with the addition of AGEs at final concentrations of 50 and 100 mg/L for 24, 48, and 72 h. AGEs in the
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Registered trials
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