Literature DB >> 2007434

Strain difference in expression of the adult-type polycystic kidney disease gene, pcy, in the mouse.

S Nagao1, T Hibino, Y Koyama, T Marunouchi, H Konishi, H Takahashi.   

Abstract

DBA/2FG-pcy and C57BL/6FG-pcy congenic strains were established by transferring the polycystic kidney disease gene, pcy, to DBA/2 and C57BL/6 mice. We carried out pathological and hematological examinations of these strains at 4, 8, 16 and 30 weeks of age. In DBA/2FG-pcy mice more than 8 weeks of age, macroscopic renal cysts were observed on the surface of both kidneys. Their kidneys weight was significantly greater than in DBA/2 mice at all ages examined. Microscopic renal cysts were evenly distributed at 4, 8 and 16 weeks of age. At 30 weeks of age, the kidneys were filled with numerous polycysts. In C57BL/6FG-pcy mice, no macroscopic renal cysts were found until the animals were 30 weeks old, and the weight of their kidneys was greater than in B6 mice of the same age. From 8 weeks of age on, a limited number of microscopic renal cysts was observed, and many renal cysts were found adjacent to the enlarged Bowman's capsules. With age, the red blood cell count and hematocrit level decreased while the platelet count increased in both strains, with greater changes occurring in DBA/2FG-pcy mice than in C57 BL/6FG-pcy mice. These findings demonstrate that polycystic kidney disease exhibits strain differences in animals with a DBA/2 and C57BL/6 background. Our results suggest that phenotypic expression of the pcy gene in the mouse depends on genetic background, and that variations in the severity of human polycystic kidney disease may be explained, at least in part, by individual differences in genetic background.

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Year:  1991        PMID: 2007434     DOI: 10.1538/expanim1978.40.1_45

Source DB:  PubMed          Journal:  Jikken Dobutsu        ISSN: 0007-5124


  6 in total

1.  Genetic identification of two major modifier loci of polycystic kidney disease progression in pcy mice.

Authors:  D D Woo; D K Nguyen; N Khatibi; P Olsen
Journal:  J Clin Invest       Date:  1997-10-15       Impact factor: 14.808

2.  Loss of PKD1 and loss of Bcl-2 elicit polycystic kidney disease through distinct mechanisms.

Authors:  P Hughes; M Robati; W Lu; J Zhou; A Strasser; P Bouillet
Journal:  Cell Death Differ       Date:  2005-11-11       Impact factor: 15.828

3.  The SAM domain of ANKS6 has different interacting partners and mutations can induce different cystic phenotypes.

Authors:  Zeineb Bakey; Marie-Thérèse Bihoreau; Rémi Piedagnel; Laure Delestré; Catherine Arnould; Alexandre d'Hotman de Villiers; Olivier Devuyst; Sigrid Hoffmann; Pierre Ronco; Dominique Gauguier; Brigitte Lelongt
Journal:  Kidney Int       Date:  2015-06-03       Impact factor: 10.612

4.  Genetic mapping of the polycystic kidney gene, pcy, on mouse chromosome 9.

Authors:  S Nagao; T Watanabe; N Ogiso; T Marunouchi; H Takahashi
Journal:  Biochem Genet       Date:  1995-12       Impact factor: 1.890

5.  Abnormal lipid and fatty acid compositions of kidneys from mice with polycystic kidney disease.

Authors:  H M Aukema; T Yamaguchi; H Takahashi; B Celi; B J Holub
Journal:  Lipids       Date:  1992-06       Impact factor: 1.880

6.  Murine Joubert syndrome reveals Hedgehog signaling defects as a potential therapeutic target for nephronophthisis.

Authors:  Ann Marie Hynes; Rachel H Giles; Shalabh Srivastava; Lorraine Eley; Jennifer Whitehead; Marina Danilenko; Shreya Raman; Gisela G Slaats; John G Colville; Henry Ajzenberg; Hester Y Kroes; Peter E Thelwall; Nicholas L Simmons; Colin G Miles; John A Sayer
Journal:  Proc Natl Acad Sci U S A       Date:  2014-06-19       Impact factor: 11.205

  6 in total

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