ArticleThe American journal of pathology2010
Deletion of von Hippel-Lindau in glomerular podocytes results in glomerular basement membrane thickening, ectopic subepithelial deposition of collagen {alpha}1{alpha}2{alpha}1(IV), expression of neuroglobin, and proteinuria.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- VHL Suppresses Angiogenesis Through HIF-1a-Mediated Ang/Tie2/AMPK/VEGF Signaling Pathway in Tie-2 Expressed Macrophages (TEMs).Biochemical genetics · 2026Article
- A New Prospect for the Treatment of Nephrotic Syndrome Based on Network Pharmacology Analysis.Current research in physiology · 2022Article
- Profile of Podocyte Translatome During Development of Type 2 and Type 1 Diabetic Nephropathy Using Podocyte-Specific TRAP mRNA RNA-seq.Diabetes · 2021Article
- Detrimental effects of hypoxia on glomerular podocytes.Journal of physiology and biochemistry · 2021Review
- EndothelialJournal of the American Society of Nephrology : JASN · 2017Article
- Hypoxia-inducible factor-1α promotes glomerulosclerosis and regulates COL1A2 expression through interactions with Smad3.Kidney international · 2016Article
- Podocytes.F1000Research · 2016Review
- von Hippel-Lindau gene plays a role during zebrafish pronephros development.In vitro cellular & developmental biology. Animal · 2015Article
- Article
- Discovery of new glomerular disease-relevant genes by translational profiling of podocytes in vivo.Kidney international · 2014Article
- Update on crescentic glomerulonephritis.Seminars in immunopathology · 2014Review
- Von Hippel-Lindau disease (VHL): a need for a murine model with retinal hemangioblastoma.Histology and histopathology · 2012Review
- Interactions between vascular endothelial growth factor and neuroglobin.Neuroscience letters · 2012Article
- Hypoxia-inducible factor-1 and neuroglobin expression.Neuroscience letters · 2012Article
- The glomerular basement membrane as a model system to study the bioactivity of heparan sulfate glycosaminoglycans.Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada · 2012Review
- Hypoxia decreases podocyte expression of slit diaphragm proteins.International journal of nephrology and renovascular disease · 2012Article
- PAPSS2 promotes alkaline phosphates activity and mineralization of osteoblastic MC3T3-E1 cells by crosstalk and Smads signal pathways.PloS one · 2012Article
- Collagen XXIV (Col24α1) promotes osteoblastic differentiation and mineralization through TGF-β/Smads signaling pathway.International journal of biological sciences · 2012Article
- Type IV collagen-initiated signals provide survival and growth cues required for liver metastasis.Oncogene · 2011Article
- Notch signaling regulates remodeling and vessel diameter in the extraembryonic yolk sac.BMC developmental biology · 2011Article
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8 authors at 2 institutions in 1 country.
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Abstract
Vascular endothelial growth factor, which is critical for blood vessel formation, is regulated by hypoxia inducible transcription factors (HIFs). A component of the E3 ubiquitin ligase complex, von Hippel-Lindau (VHL) facilitates oxygen-dependent polyubiquitination and proteasomal degradation of HIFalpha subunits. Hypothesizing that deletion of podocyte VHL would result in HIFalpha hyperstabilization, we crossed podocin promoter-Cre transgenic mice, which express Cre recombinase in podocytes beginning at the capillary loop stage of glomerular development, with floxed VHL mice. Vascular patterning and glomerular development appeared unaltered in progeny lacking podocyte VHL. However, urinalysis showed increased albumin excretion by 4 weeks when compared with wild-type littermates with several sever cases (>1000 microg/ml). Many glomerular ultrastructural changes were seen in mutants, including focal subendothelial delamination and widespread podocyte foot process broadening, and glomerular basement membranes (GBMs) were significantly thicker in 16-week-old mutants compared with controls. Moreover, immunoelectron microscopy showed ectopic deposition of collagen alpha1alpha2alpha1(IV) in GBM humps beneath podocytes. Significant increases in the number of Ki-67-positive mesangial cells were also found, but glomerular WT1 expression was significantly decreased, signifying podocyte death and/or de-differentiation. Indeed, expression profiling of mutant glomeruli suggested a negative regulatory feedback loop involving the HIFalpha prolyl hydroxylase, Egln3. In addition, the brain oxygen-binding protein, Neuroglobin, was induced in mutant podocytes. We conclude that podocyte VHL is required for normal maintenance of podocytes, GBM composition and ultrastructure, and glomerular barrier properties.
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