ArticleMolecular vision2012
Decreased K5 receptor expression in the retina, a potential pathogenic mechanism for diabetic retinopathy.
Article in Molecular vision, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 6 citations in OpenAlex.
- Poly(ADP-Ribose) Polymerase-1 (PARP-1) Inhibitors Reduce Reactive Gliosis and Improve Angiostatin Levels in Retina of Diabetic Rats.Neurochemical research · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePlasminogen kringle 5 (K5) is a potent angiogenic inhibitor and specifically binds to the voltage-dependent anion channel believed to function as the K5 receptor (K5R). To investigate the role of K5R in diabetic retinopathy, the present study measured the expression levels of K5R in the retina of diabetic retinopathy models. In cultured retinal Müller cells, K5 inhibited vascular endothelial growth factor (VEGF) expression as shown with enzyme-linked immunosorbent assay and western blot analysis, suggesting that K5 has a direct effect on Müller cells.
methodsTo identify K5R in retinal Müller cells, ligand binding and competition assays as well as real-time reverse transcriptional polymerase chain reaction were performed in Müller cells. (125)I-K5 showed saturable binding to cultured Müller cells. The binding can be competed off by an excess amount of unlabeled K5 but not by angiostatin, demonstrating the specificity of the K5 binding to Müller cells. Consistent with the binding assay, reverse transcriptional polymerase chain reaction using voltage-dependent anion channel-specific primers detected the K5R mRNA in the Müller cells.
resultsInterestingly, K5R mRNA expression in Müller cells was downregulated by diabetic conditions including hypoxia and high glucose medium. Incubation with K5 ligand prevented hypoxia-induced downregulation of K5R. Furthermore, K5R expression was also downregulated in the retina of the oxygen-induced retinopathy model, a model of ischemia-induced retinal neovascularization. In a type 1 diabetic rat model, K5R expression in the retina was significantly suppressed in rats that had diabetes for 5 and 8 weeks.
conclusionsThese results suggest that K5R is expressed in retinal Müller cells, which may mediate the inhibitory effect of K5 on VEGF expression. In diabetes conditions, K5R expression levels are decreased in the retina, which could contribute to the VEGF overexpression in diabetic retinopathy. These findings suggest that the decreased levels of K5R may also play a pathogenic role in diabetic retinopathy.
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Identifiers
22355244PMC3283210W2125391007What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.