ArticleThe American journal of pathology2010
Induction of podocyte VEGF164 overexpression at different stages of development causes congenital nephrosis or steroid-resistant nephrotic syndrome.
Article in The American journal of pathology, 2010. 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, 45 citations in OpenAlex.
- The role of cellular crosstalk in the progression of diabetic nephropathy.Frontiers in endocrinology · 2023Review
- Glomerular Endothelial Cell-Derived miR-200c Impairs Glomerular Homeostasis by Targeting Podocyte VEGF-A.International journal of molecular sciences · 2022Article
- BECLIN1 Is Essential for Podocyte Secretory Pathways Mediating VEGF Secretion and Podocyte-Endothelial Crosstalk.International journal of molecular sciences · 2022Article
- Serum IL-12p40: A novel biomarker for early prediction of minimal change disease relapse following glucocorticoids therapy.Frontiers in medicine · 2022Article
- Role of Endothelial Glucocorticoid Receptor in the Pathogenesis of Kidney Diseases.International journal of molecular sciences · 2021Review
- Rho-GTPase Activating Protein myosin MYO9A identified as a novel candidate gene for monogenic focal segmental glomerulosclerosis.Kidney international · 2021Article
- Vascular Endothelial Growth Factor (VEGF) and Neopterin Levels in Children with Steroid-sensitive and Steroid-resistant Nephrotic Syndrome.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2021Article
- Nephrotic syndrome in a dish: recent developments in modeling in vitro.Pediatric nephrology (Berlin, Germany) · 2020Review
- Podocyte histone deacetylase activity regulates murine and human glomerular diseases.The Journal of clinical investigation · 2019Article
- Forced expression of vascular endothelial growth factor-A in podocytes decreases mesangial cell numbers and attenuates endothelial cell differentiation in the mouse glomerulus.Clinical and experimental nephrology · 2018Article
- Modulation of VEGF-A Alternative Splicing as a Novel Treatment in Chronic Kidney Disease.Genes · 2018Review
- Article
- Therapeutic angiogenesis by vascular endothelial growth factor supplementation for treatment of renal disease.Current opinion in nephrology and hypertension · 2016Review
- Blood vessel crosstalk during organogenesis-focus on pancreas and endothelial cells.Wiley interdisciplinary reviews. Developmental biology · 2016Review
- Stability and Species Specificity of Renal VEGF-A Splicing Patterns in Kidney Disease.PloS one · 2016Article
- Expression of VEGF in neonatal urinary obstruction: does expression of VEGF predict hydronephrosis?Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Review series: The cell biology of renal filtration.The Journal of cell biology · 2015Review
- Glomerular endothelial cell injury and cross talk in diabetic kidney disease.American journal of physiology. Renal physiology · 2015Review
- A novel adenoviral vector carrying an all-in-one Tet-On system with an autoregulatory loop for tight, inducible transgene expression.BMC biotechnology · 2015Article
- Article
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8 authors at 4 institutions in 1 country.
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Abstract
The tight regulation of vascular endothelial growth factor-A (VEGF-A) signaling is required for both the development and maintenance of the glomerular filtration barrier, but the pathogenic role of excessive amounts of VEGF-A detected in multiple renal diseases remains poorly defined. We generated inducible transgenic mice that overexpress podocyte VEGF164 at any chosen stage of development. In this study, we report the phenotypes that result from podocyte VEGF164 excess during organogenesis and after birth. On doxycycline induction, podocin-rtTA:tet-O-VEGF164 mice express twofold higher kidney VEGF164 levels than single transgenic mice, localized to podocytes. Podocyte VEGF164 overexpression during organogenesis resulted in albuminuria at birth and was associated with glomerulomegaly, uniform podocyte effacement, very few and wide foot processes joined by occluding junctions, almost complete absence of slit diaphragms, and swollen endothelial cells with few fenestrae as revealed by transmission electron microscopy. Podocyte VEGF164 overexpression after birth caused massive albuminuria in 70% of 2-week-old mice, glomerulomegaly, and minimal changes on light microscopy. Transmission electron microscopy showed podocyte effacement and fusion and morphologically normal endothelial cells. Podocyte VEGF164 overexpression induced nephrin down-regulation without podocyte loss. VEGF164-induced abnormalities were reversible on removal of doxycycline and were unresponsive to methylprednisolone. Collectively, the data suggest that moderate podocyte VEGF164 overexpression during organogenesis results in congenital nephrotic syndrome, whereas VEGF164 overexpression after birth induces a steroid-resistant minimal change like-disease in mice.
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