ArticleThe American journal of pathology2010
Inducible nephrin transgene expression in podocytes rescues nephrin-deficient mice from perinatal death.
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 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Gene modification: Exploring the potential in treating kidney diseases.Pharmacological research · 2026Review
- Cell and gene therapy for kidney disease.Nature reviews. Nephrology · 2023Review
- Aberrantly glycosylated IgG elicits pathogenic signaling in podocytes and signifies lupus nephritis.JCI insight · 2021Article
- Recent advances of animal model of focal segmental glomerulosclerosis.Clinical and experimental nephrology · 2018Review
- Proteinuric Kidney Diseases: A Podocyte's Slit Diaphragm and Cytoskeleton Approach.Frontiers in medicine · 2018Review
- Pituitary adenylate cyclase-activating polypeptide (PACAP) in zebrafish models of nephrotic syndrome.PloS one · 2017Article
- Nephrin Tyrosine Phosphorylation Is Required to Stabilize and Restore Podocyte Foot Process Architecture.Journal of the American Society of Nephrology : JASN · 2016Article
- Nephrin Preserves Podocyte Viability and Glomerular Structure and Function in Adult Kidneys.Journal of the American Society of Nephrology : JASN · 2015Article
- Animal models of nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2013Review
- Focal segmental glomerulosclerosis is induced by microRNA-193a and its downregulation of WT1.Nature medicine · 2013Article
- The Extract of Litsea japonica Reduced the Development of Diabetic Nephropathy via the Inhibition of Advanced Glycation End Products Accumulation in db/db Mice.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- New perspectives on the renal slit diaphragm protein podocin.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2011Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations leading to nephrin loss result in massive proteinuria both in humans and mice. Early perinatal lethality of conventional nephrin knockout mice makes it impossible to determine the role of nephrin protein in the adult kidney and in extra-renal tissues. Herein, we studied whether podocyte-specific, doxycycline-inducible, rat nephrin expression can rescue nephrin-deficient mice from perinatal lethality. Fourteen littermates out of 72 lacked endogenous nephrin and expressed transgenic rat nephrin. Six of these rescued mice survived until 6 weeks of age, whereas the nephrin-deficient pups died before the age of 5 days. The rescued mice were smaller, developed proteinuria, and showed histological abnormalities in the kidney. Despite foot process effacement, slit diaphragms were observed. Importantly, the expression and localization of several proteins associated with the signaling capacity of nephrin or the regulation of the expression of nephrin were changed in the podocytes. Indeed, all rescued mice showed impaired locomotor activity and distinct histological abnormalities in the cerebellum, and the male mice were also infertile and showed genital malformations. These observations are consistent with normal nephrin expression in the testis and cerebellum. These observations indicate that podocyte-specific expression of rat nephrin can rescue nephrin-deficient mice from perinatal death, but is not sufficient for full complementation.
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