ArticlePloS one2018
Advanced glycation end (AGE) product modification of laminin downregulates Kir4.1 in retinal Müller cells.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Stage-Associated Cellular and Molecular Signatures in Diabetic Retinopathy Identified Through Integrated Bulk and Single-Cell Transcriptomic Analysis.International journal of molecular sciences · 2026Article
- The roles of advanced glycation end products in cardiovascular diseases: from mechanisms to therapeutic strategies.Frontiers in cardiovascular medicine · 2025Review
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- Article
- The mechanics of the retina: Müller glia role on retinal extracellular matrix and modelling.Frontiers in medicine · 2024Review
- The Role of Müller Cells in Diabetic Macular Edema.Investigative ophthalmology & visual science · 2023Review
- Kir4.1 may represent a novel therapeutic target for diabetic retinopathy (Review).Experimental and therapeutic medicine · 2021Review
- Current understanding of the molecular and cellular pathology of diabetic retinopathy.Nature reviews. Endocrinology · 2021Review
- Glycation of fibronectin inhibits VEGF-induced angiogenesis by uncoupling VEGF receptor-2-c-Src crosstalk.Journal of cellular and molecular medicine · 2020Article
- VEGF Upregulates EGFR Expression to Stimulate Chemotactic Behaviors in the rMC-1 Model of Müller Glia.Brain sciences · 2020Article
- Rescue of Defective Electroretinographic Responses in Dp71-Null Mice With AAV-Mediated Reexpression of Dp71.Investigative ophthalmology & visual science · 2020Article
- Nutritional ketosis as an intervention to relieve astrogliosis: Possible therapeutic applications in the treatment of neurodegenerative and neuroprogressive disorders.European psychiatry : the journal of the Association of European Psychiatrists · 2020Review
- The Diurnal Rhythm of Insulin Receptor Substrate-1 (IRS-1) and Kir4.1 in Diabetes: Implications for a Clock Gene Bmal1.Investigative ophthalmology & visual science · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Diabetic retinopathy (DR) is a major cause of adult blindness. Retinal Müller cells maintain water homeostasis and potassium concentration via inwardly rectifying Kir4.1 channels. Accumulation of advanced glycation end products (AGEs) is a major pathologic event in DR. While diabetes leads to a decrease in the Kir4.1 channels, it remains unknown whether AGEs-linked to the basement membrane (BM) affect normal Kir4.1 channels. For this study, we hypothesized that AGE-modification of laminin is detrimental to Kir4.1 channels, therefore, disrupting Müller cell function. The AGE-modified laminin-coated substrates were prepared by incubating Petri-dishes with laminin and methylglyoxal for seven days. The rat Müller cells (rMC-1) were propagated on AGE-modified laminin, and Kir4.1 expression and function were evaluated. Quantification of AGEs using ELISA revealed a dose-dependent increase in methylglyoxal-hydro-imidazolone adducts. The rMC-1 propagated on AGE-modified laminin demonstrated a decrease in Kir4.1 levels in immunofluorescence and western blot studies and a decrease in the Kir4.1 channel function. Kir4.1 decrease on AGE-modified laminin resulted in a disorganization of an actin cytoskeleton and disruption of α-dystroglycan-syntrophin-dystrophin complexes. Our studies suggest that AGE-modification of laminin is detrimental to Kir4.1 channels. By studying the role of AGEs in Kir4.1 channels we have identified a novel mechanism of Müller cell dysfunction and its subsequent involvement in DR.
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Registered trials
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