ArticleJournal of molecular medicine (Berlin, Germany)2010
High-glucose and advanced glycosylation end products increased podocyte permeability via PI3-K/Akt signaling.
Article in Journal of molecular medicine (Berlin, Germany), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Exploring the renoprotective potential of Beta vulgaris in diabetic nephropathy: an integrated network pharmacology, molecular docking and dynamics simulation study.Molecular diversity · 2026Article
- Crosstalk between ferroptosis and innate immune in diabetic kidney disease: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Identification of miRNAs-genes regulatory network in diabetic nephropathy based on bioinformatics analysis.Medicine · 2019Article
- Montelukast improves the changes of cytoskeletal and adaptor proteins of human podocytes by interleukin-13.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- Effects of interleukin-13 and montelukast on the expression of zonula occludens-1 in human podocytes.Yonsei medical journal · 2015Article
- Article
- Roles of adaptor proteins in podocyte biology.World journal of nephrology · 2013Review
- Angiotensin II suppresses adenosine monophosphate-activated protein kinase of podocytes via angiotensin II type 1 receptor and mitogen-activated protein kinase signaling.Clinical and experimental nephrology · 2013Article
- Puromycin aminonucleoside modulates p130Cas of podocytes.Korean journal of pediatrics · 2012Article
- Ginseng total saponin improves podocyte hyperpermeability induced by high glucose and advanced glycosylation endproducts.Journal of Korean medical science · 2011Article
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
Regardless of the underlying disease, the proteinuric condition demonstrates ultrastructural changes in podocytes with retraction and effacement of the highly specialized interdigitating foot processes. To investigate how high-glucose (HG) and advanced glycosylation end products (AGE) induce podocyte phenotypical changes, including quantitative and distributional changes of zonula occludens (ZO)-1 protein and search for the signaling mechanisms, we cultured rat glomerular epithelial cells (GEpC) and mouse podocytes under: (1) normal glucose (5 mM, control); (2) HG (30 mM); (3) AGE-added; or (4) HG plus AGE-added conditions. HG plus AGE increased the permeability of monolayered GEpCs and induced ultrastructural separation between confluent GEpCs. ZO-1 moved to inner actin filament complexes in both AGE- and/or HG by confocal imaging. HG plus AGE-added condition also decreased ZO-1 protein amount and mRNA expression compared to normal glucose or osmotic control conditions. We could also confirm the induction of RAGE (receptor for AGE) and PI3-K/Akt signaling pathway by AGE and HG. In addition, LY294002, a PI3-K inhibitor, could prevent the quantitative and distributional changes of ZO-1 and RAGE and the increased permeability induced by HG and AGE. These findings suggest that diabetic conditions induce the podocyte ZO-1 changes via RAGE and PI3-K/Akt signaling, leading to increased permeability.
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