1998 Fiscal Year Final Research Report Summary
The studies for modifier-genes on the progression of polycystic kidney cliseasl in mice.
| Project/Area Number |
08459025
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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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 University School of Medicine, Hygiene, Professor, 衛生学部, 教授 (80084606)
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| Project Period (FY) |
1996 – 1998
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| Keywords | DBA / 2FG-pcy / C57BL / 6FG-pcy / congenic strain / Reconbinant Congenic / PKD / model animal / pcR / modifier-genes |
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| Research Abstract |
Polycystic kidney disense (PKD) is one of the most common hereditary renal disorders. The disease, characterized by the development of cysts that are derived from renal tubules in the cortsx and medulla, leads to bilatal kidney enlargement and renal failute. Autsomal donivat PKD(ADPKD) is characterized by rektively slow progression over many decades. Two different gene, PKD1(chromosome 16p13.3) and PKD2(charomosome 4q21-22), have been mapped and cloned in human ADPKD.
In rodent models of slowly progressive PKD, the rate of kidney enlargement and functional decline can be diminished by the adoministration of anti-inflammatory storoids such as methyl prednisolone, low protein diets, NaHCO_3, KHCO_3, or potassium citrate/citric acid, soy been enriched diets and inhibitors of angiotensim-converting enzyme.
An autosomal recessive gene (pcy) on mouse chromosone 9 couses variable reval cystic disease when expressed on a DBA/2 background. On the C57B46 background, pcy gene expression induces a much less severe disease, but the time for full development is impractical.
Now we have not found that the modifier-genes on mouse chromose 4 and 16 were associated with the development of cysts. Those findings worrant futher imvestigation of madifier-geves in other chromoses.
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