ArticleJournal of the American Society of Nephrology : JASN2017
Inducible Expression of Claudin-1 in Glomerular Podocytes Generates Aberrant Tight Junctions and Proteinuria through Slit Diaphragm Destabilization.
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- Structural and functional insights of the podocyte slit diaphragm complex.Tissue barriers · 2026Review
- Cdc42 Activation in Antinephrin Antibody-Induced Nephropathy.Journal of the American Society of Nephrology : JASN · 2025Article
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- Identification of Anoikis-Related Genes in Chronic Kidney Disease Based on Bioinformatics Analysis Combined with Experimental Validation.Journal of inflammation research · 2025Article
- Cross Talk Between Macrophages and Podocytes in Diabetic Nephropathy: Potential Mechanisms and Novel Therapeutics.Mediators of inflammation · 2025Review
- Ability of NAD and Sirt1 to epigenetically suppress albuminuria.Clinical and experimental nephrology · 2024Review
- Evaluating the State of Glomerular Disease by Analyzing Urinary Sediments: mRNA Levels and Immunofluorescence Staining for Various Markers.International journal of molecular sciences · 2024Article
- Evaluation of glomerular sirtuin-1 and claudin-1 in the pathophysiology of nondiabetic focal segmental glomerulosclerosis.Scientific reports · 2023Article
- Cellular crosstalk of mesangial cells and tubular epithelial cells in diabetic kidney disease.Cell communication and signaling : CCS · 2023Review
- The role of claudins in homeostasis.Nature reviews. Nephrology · 2023Review
- Tight junction disruption and the pathogenesis of the chronic complications of diabetes mellitus: A narrative review.World journal of diabetes · 2023Review
- Spatial composition and turnover of the main molecules in the adult glomerular basement membrane.Tissue barriers · 2023Review
- Nicotinamide mononucleotide ameliorates adriamycin-induced renal damage by epigenetically suppressing the NMN/NAD consumers mediated by Twist2.Scientific reports · 2022Article
- Claudins in kidney health and disease.Kidney research and clinical practice · 2022Article
- NADInternational journal of molecular sciences · 2022Article
- Article
- The effect of tropisetron on oxidative stress, SIRT1, FOXO3a, and claudin-1 in the renal tissue of STZ-induced diabetic rats.Cell stress & chaperones · 2021Article
- Global transcriptomic changes occur in aged mouse podocytes.Kidney international · 2020Article
- Decreased Urinary Levels ofInternational journal of molecular sciences · 2020Article
- New insight into podocyte slit diaphragm, a therapeutic target of proteinuria.Clinical and experimental nephrology · 2020Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The tight junction (TJ) has a key role in regulating paracellular permeability to water and solutes in the kidney. However, the functional role of the TJ in the glomerular podocyte is unclear. In diabetic nephropathy, the gene expression of claudins, in particular claudin-1, is markedly upregulated in the podocyte, accompanied by a tighter filtration slit and the appearance of TJ-like structures between the foot processes. However, there is no definitive evidence to show slit diaphragm (SD) to TJ transition in vivo Here, we report the generation of a claudin-1 transgenic mouse model with doxycycline-inducible transgene expression specifically in the glomerular podocyte. We found that induction of claudin-1 gene expression in mature podocytes caused profound proteinuria, and with deep-etching freeze-fracture electron microscopy, we resolved the ultrastructural change in the claudin-1-induced SD-TJ transition. Notably, immunolabeling of kidney proteins revealed that claudin-1 induction destabilized the SD protein complex in podocytes, with significantly reduced expression and altered localization of nephrin and podocin proteins. Mechanistically, claudin-1 interacted with both nephrin and podocin through cis- and trans-associations in cultured cells. Furthermore, the rat puromycin aminonucleoside nephrosis model, previously suspected of undergoing SD-TJ transition, exhibited upregulated expression levels of claudin-1 mRNA and protein in podocytes. Together, our data attest to the novel concept that claudins and the TJ have essential roles in podocyte pathophysiology and that claudin interactions with SD components may facilitate SD-TJ transition that appears to be common to many nephrotic conditions.
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