ArticleThe Journal of veterinary medical science2016
Tensin2-deficient mice on FVB/N background develop severe glomerular disease.
Article in The Journal of veterinary medical science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
- Quantitative phenotyping ofAmerican journal of physiology. Renal physiology · 2024Article
- Tensins in Kidney Function and Diseases.Life (Basel, Switzerland) · 2023Review
- Tensin 2-deficient nephropathy: mechanosensitive nephropathy, genetic susceptibility.Experimental animals · 2022Review
- The versatile electric condition in mouse embryos for genome editing using a three-step square-wave pulse electroporator.Experimental animals · 2022Article
- Positive correlation between renal tubular flattening and renal tubular injury/interstitial fibrosis in murine kidney disease models.The Journal of veterinary medical science · 2021Article
- Tensins - emerging insights into their domain functions, biological roles and disease relevance.Journal of cell science · 2021Review
- RecessiveScience advances · 2021Article
- Recurrent Urinary Tract Infection: A Mystery in Search of Better Model Systems.Frontiers in cellular and infection microbiology · 2021Review
- Deletion of the Tensin2 SH2-PTB domain, but not the loss of its PTPase activity, induces podocyte injury in FVB/N mouse strain.Experimental animals · 2020Article
- Tensin regulates pharyngeal pumping in Caenorhabditis elegans.Biochemical and biophysical research communications · 2020Article
- PTEN-induced partial epithelial-mesenchymal transition drives diabetic kidney disease.The Journal of clinical investigation · 2019Article
- C1r/C1s deficiency is insufficient to induce murine systemic lupus erythematosus.Genes and immunity · 2019Article
- Genetics of Childhood Steroid Sensitive Nephrotic Syndrome: An Update.Frontiers in pediatrics · 2019Review
- Genetic loci for resistance to podocyte injury caused by the tensin2 gene deficiency in mice.BMC genetics · 2018Article
- C1-Ten is a PTPase of nephrin, regulating podocyte hypertrophy through mTORC1 activation.Scientific reports · 2017Article
- Down-regulation of tensin2 enhances tumorigenicity and is associated with a variety of cancers.Oncotarget · 2016Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tensin2 (Tns2) is an essential component for the maintenance of glomerular basement membrane (GBM) structures. Tns2-deficient mice were previously shown to develop mild glomerular injury on a DBA/2 background, but not on a C57BL/6J or a 129/SvJ background, suggesting that glomerular injury by the deletion of Tns2 was strongly dependent on the genetic background. To further understand the mechanisms for the onset and the progression of glomerular injury by the deletion of Tns2, we generated Tns2-deficient mice on an FVB/N (FVB) strain, which is highly sensitive to glomerular disease. Tns2-deficient mice on FVB (FVBGN) developed severe nephrotic syndrome, and female FVBGN mice died within 8 weeks. Ultrastructural analysis revealed that FVBGN mice exhibited severe glomerular defects with mesangial process invasion of glomerular capillary tufts, lamination and thickening of the GBM and subsequent podocyte foot process effacement soon after birth. Aberrant laminin components containing α1, α2 and β1 chains, which are normally expressed in the mesangium, accumulated in the GBM of FVBGN, suggesting that these components originated from mesangial cells that invaded glomerular capillary tufts. Compared to Tns2-deficient mice on the other backgrounds in previous reports, FVBGN mice developed earlier onset of glomerular defects and rapid progression of renal failure. Thus, this study further extended our understanding of the possible genetic background effect on the deterioration of nephrotic syndrome by Tns2 deficiency.
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