ArticlePloS one2013
1,25-dihydroxyvitamin D(3) inhibits podocyte uPAR expression and reduces proteinuria.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Article
- APOL1 Modulates Renin-Angiotensin System.Biomolecules · 2024Article
- suPAR and WT1 modify the adhesion of podocytes and are related to proteinuria in class IV lupus nephritis.Journal of translational autoimmunity · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- The Perspective of Vitamin D on suPAR-Related AKI in COVID-19.International journal of molecular sciences · 2022Review
- Vitamin D and Glomerulonephritis.Medicina (Kaunas, Lithuania) · 2021Review
- The Plasma Soluble Urokinase Plasminogen Activator Receptor Is Related to Disease Activity of Patients with ANCA-Associated Vasculitis.Mediators of inflammation · 2020Article
- WWC1 promotes podocyte survival via stabilizing slit diaphragm protein dendrin.Molecular medicine reports · 2017Article
- Serum 1,25-dihydroxyvitamin D Better Reflects Renal Parameters Than 25-hydoxyvitamin D in Patients with Glomerular Diseases.International journal of medical sciences · 2017Article
- New Pathogenic Concepts and Therapeutic Approaches to Oxidative Stress in Chronic Kidney Disease.Oxidative medicine and cellular longevity · 2016Review
- Soluble Urokinase Receptors in Focal Segmental Glomerulosclerosis: A Review on the Scientific Point of View.Journal of immunology research · 2016Review
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccumulating studies have demonstrated that 1,25-Dihydroxyvitamin D(3) (1,25(OH)2D3) reduces proteinuria and protects podocytes from injury. Recently, urokinase receptor (uPAR) and its soluble form have been shown to cause podocyte injury and focal segmental glomerulosclerosis (FSGS). Here, our findings showed that 1,25(OH)2D3 did inhibit podocyte uPAR expression and attenuate proteinuria and podocyte injury. METHODOLOGY/PRINCIPAL
findingsIn this study, the antiproteinuric effect of 1,25(OH)2D3 was examined in the lipopolysaccharide mice model of transient proteinuria (LPS mice) and in the 5/6 nephrectomy rat FSGS model(NTX rats). uPAR protein expression were tested by flow cytometry, immune cytochemistry and western blot analysis, and uPAR mRNA expression by real-time quantitative PCR in cultured podocytes and kidney glomeruli isolated from mice and rats. Podocyte motility was observed by transwell migration assay and wound healing assay. Podocyte foot processes effacement was identified by transmission electron microscopy. We found that 1,25(OH)2D3 inhibited podocyte uPAR mRNA and protein synthesis in LPS-treated podocytes, LPS mice and NTX rats, along with 1,25(OH)2D3 reducing proteinuria in NTX rats and LPS mice.1,25(OH)2D3 reduced glomerulosclerosis in NTX rats and alleviated podocyte foot processes effacement in LPS mice. Transwell migration assay and wound healing assay showed that LPS-induced podocyte motility, irrespective of random or directed motility, were substantially reduced by 1,25(OH)2D3. CONCLUSIONS/SIGNIFICANCE: Our results demonstrated that 1,25(OH)2D3 inhibited podocyte uPAR expression in vitro and in vivo, which may be an unanticipated off target effect of 1,25(OH)2D3 and explain its antiproteinuric effect in the 5/6 nephrectomy rat FSGS model and the LPS mouse model of transient proteinuria.
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