ArticlePediatric nephrology (Berlin, Germany)1988
Congenital murine polycystic kidney disease. II. Pathogenesis of tubular cyst formation.
Article in Pediatric nephrology (Berlin, Germany), 1988. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 53 citations in OpenAlex.
- Reduction of elevated Gli3 does not alter the progression of autosomal recessive polycystic kidney disease.Physiological reports · 2025Article
- The Biological Significance and Implications of Planar Cell Polarity for Nephrology.Frontiers in physiology · 2021Review
- Acceleration of polycystic kidney disease progression in cpk mice carrying a deletion in the homeodomain protein Cux1.American journal of physiology. Renal physiology · 2008Article
- Cystin, a novel cilia-associated protein, is disrupted in the cpk mouse model of polycystic kidney disease.The Journal of clinical investigation · 2002Article
- Differential rescue of the renal and hepatic disease in an autosomal recessive polycystic kidney disease mouse mutant. A new model to study the liver lesion.The American journal of pathology · 1997Article
- Renal and biliary abnormalities in a new murine model of autosomal recessive polycystic kidney disease.Pediatric nephrology (Berlin, Germany) · 1993Article
- Abnormal sodium pump distribution during renal tubulogenesis in congenital murine polycystic kidney disease.Proceedings of the National Academy of Sciences of the United States of America · 1992Article
- Polypeptide growth factors in metanephric growth and segmental nephron differentiation.Pediatric nephrology (Berlin, Germany) · 1990Article
- The microanatomy of the intrahepatic bile duct in polycystic disease: comparison of the cpk mouse and human.Journal of experimental pathology (Oxford, England) · 1990Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In the current study, the pathogenesis of proximal tubular cyst formation was studied in an animal model of polycystic kidney disease, the CPK mouse. The specific roles of (a) sodium-potassium adenosine triphosphatase (Na-K ATPase) activity, determined by an enzyme-linked kinetic microassay, (b) proximal tubular epithelial hyperplasia, determined by calculation of mitotic indices, and (c) altered proximal tubular basal lamina formation, determined by immunohistological localization of basal lamina glycoproteins, were investigated at progressive developmental stages of CPK proximal tubular cyst formation. Increases in renal Na-K ATPase were present at the earliest fetal stages of proximal tubular cyst formation, and subsequently paralleled the course of proximal tubular cyst progression. Proximal tubular epithelial hyperplasia, although not present at the earliest stages of cyst formation, was a consistent feature of progressive proximal tubular cystic enlargement. Abnormalities in basal lamina glycoprotein expression were not present at any stage of proximal tubular cyst development. We conclude that increased Na-K ATPase and tubular epithelial hyperplasia are significant features of proximal tubular cyst formation in the CPK mouse.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.