1992 Fiscal Year Final Research Report Summary
Study of the pathogenesis of progressive hereditary PKD mouse
| Project/Area Number |
02455026
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
広領域
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| Research Institution | Fujita Health University |
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Principal Investigator |
TAKAHASHI Hisahide Fujita Health Univ., Health Sciences, Professor, 衛生学部, 教授 (80084606)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAO Shizuko Fujita Health Univ., Inst. for Comprehensive Med. Sci., Researcher, 総合医科学研究所, 研究員 (20183527)
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| Project Period (FY) |
1990 – 1992
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| Keywords | Polycystic Kidney / Strain Difference / DBA / 2FG-pcy / C57BL / 6FG-pcy / Genetic Background / ADPKD / Animal Models / Aneurysms |
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| Research Abstract |
DBA/2FG-pcy and C57BL/6FG-pcy congenic strain 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 strain 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, 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 C57BL/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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