ArticleAmerican journal of nephrology2015
Deletion of UNC5B in Kidney Epithelium Exacerbates Diabetic Nephropathy in Mice.
Article in American journal of nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Netrin-1 works with UNC5B to regulate angiogenesis in diabetic kidney disease.Frontiers of medicine · 2020Article
- Cellular Recruitment by Podocyte-Derived Pro-migratory Factors in Assembly of the Human Renal Filter.iScience · 2019Article
- Acute Kidney Injury and Progression of Diabetic Kidney Disease.Advances in chronic kidney disease · 2018Review
- Netrin as a Novel Biomarker and Its Therapeutic Implications in Diabetes Mellitus and Diabetes-Associated Complications.Journal of diabetes research · 2018Review
- Article
- Specific MAPK inhibitors prevent hyperglycemia-induced renal diseases in type 1 diabetic mouse model.Molecular and cellular biochemistry · 2016Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGuidance cue netrin-1 was shown to have protective effects in diabetic nephropathy. However, the role of its receptor UNC5B in diabetic kidney disease is unknown. Moreover, whether netrin-1 is protective against diabetic kidney disease in a genetic model of nephropathy and in the nephropathy prone DBA background is also unknown. The aim of this study was to determine the significance of UNC5B in tubular epithelial cells in chronic kidney disease due to diabetes and evaluate whether netrin-1 is also protective in the case of a nephropathy-prone mouse.
methodsProximal tubular epithelium-specific UNC5B knockout mice as well as heterozygous UNC5B knockout mice were used to determine the roles of UNC5B in nephropathy. Diabetes was induced in these tissue-specific knockout, heterozygous and WT mice, and albuminuria was then monitored.
resultsWT and heterozygous diabetic mice developed significant albuminuria at 8 weeks after induction of diabetes as compared to buffer-treated control mice. However, albuminuria was significantly more pronounced in mice with proximal tubule specific deletion of UNC5B. Transgenic overexpression of netrin-1 in proximal tubules in the DBA background and administration of recombinant netrin-1 to Ins2Akita mice also significantly reduced diabetes-induced albuminuria and suppressed glomerular and interstitial lesions.
conclusionOur data suggested that netrin-1 signaling in proximal tubular epithelium may play a critical role in the protection of kidney against diabetic kidney disease.
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