ArticleAmerican journal of physiology. Renal physiology2007
Nephrogenic diabetes insipidus in mice caused by deleting COOH-terminal tail of aquaporin-2.
Article in American journal of physiology. Renal physiology, 2007. 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, 24 citations in OpenAlex.
- Article
- Mechanisms of Developmental Toxicity of Dioxins and Related Compounds.International journal of molecular sciences · 2019Review
- Urinary bladder hypertrophy characteristic of male ROMK Bartter's mice does not occur in female mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Hereditary Nephrogenic Diabetes Insipidus: Pathophysiology and Possible Treatment. An Update.International journal of molecular sciences · 2017Review
- The Trafficking of the Water Channel Aquaporin-2 in Renal Principal Cells-a Potential Target for Pharmacological Intervention in Cardiovascular Diseases.Frontiers in pharmacology · 2016Review
- Genetic ablation of aquaporin-2 in the mouse connecting tubules results in defective renal water handling.The Journal of physiology · 2013Article
- Nephrogenic diabetes insipidus: essential insights into the molecular background and potential therapies for treatment.Endocrine reviews · 2013Review
- Regulation of transport in the connecting tubule and cortical collecting duct.Comprehensive Physiology · 2012Review
- Central diabetes insipidus associated with impaired renal aquaporin-1 expression in mice lacking liver X receptor β.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- A selective EP4 PGE2 receptor agonist alleviates disease in a new mouse model of X-linked nephrogenic diabetes insipidus.The Journal of clinical investigation · 2009Article
- Serine 269 phosphorylated aquaporin-2 is targeted to the apical membrane of collecting duct principal cells.Kidney international · 2009Article
- Hsp90 inhibitor partially corrects nephrogenic diabetes insipidus in a conditional knock-in mouse model of aquaporin-2 mutation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
In mammals, the hormonal regulation of water homeostasis is mediated by the aquaporin-2 water channel (Aqp2) of the collecting duct (CD). Vasopressin induces redistribution of Aqp2 from intracellular vesicles to the apical membrane of CD principal cells, accompanied by increased water permeability. Mutations of AQP2 gene in humans cause both recessive and dominant nephrogenic diabetes insipidus (NDI), a disease in which the kidney is unable to concentrate urine in response to vasopressin. In this study, we generated a line of mice with the distal COOH-terminal tail of the Aqp2 deleted (Aqp2(Delta230)), including the protein kinase A phosphorylation site (S256), but still retaining the putative apical localization signal (221-229) at the COOH-terminal. Mice heterozygous for the truncation appear normal. Homozygotes are viable to adulthood, with reduced urine concentrating capacity, increased urine output, decreased urine osmolality, and increased daily water consumption. Desmopressin increased urine osmolality in wild-type mice but had no effect on Aqp2(Delta230/Delta230) mice. Kidneys from affected mice showed CD and pelvis dilatation and papillary atrophy. By immunohistochemical and immunoblot analyses using antibody against the NH(2)-terminal region of the protein Aqp2(Delta230/Delta230) mice had a markedly reduced protein abundance. Expression of the truncated protein in MDCK cells was consistent with a small amount of functional expression but no stimulation. Thus we have generated a mouse model of NDI that may be useful in studying the physiology and potential therapy of this disease.
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