2014 Fiscal Year Research-status Report
ICGN マウスを用いた慢性腎臓病に対する抵抗性/感受性遺伝子の同定
Project/Area Number |
25430083
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Research Institution | Kitasato University |
Principal Investigator |
佐々木 宣哉 北里大学, 獣医学部, 教授 (20302614)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | ICGN mouse / chronic kidney disease / glomerulosclerosis / anemia / proteinuria |
Outline of Annual Research Achievements |
To verify the existence of the CKD-resistant loci on Chr 2 from the B6 mouse, we produced ICGN congenic mice homozygously introgressed Chr 2 from the B6 mouse using marker-assisted backcrossing. ICGN mice showed low Hb and low Ht, indicating significant renal anemia. On the other hand, the erythrocytic parameters of the congenic mice were normal levels as well as control mice. Both ICGN and congenic mice mice developed proteinuria up to 8 week old, but the urinary albumin excretion in congenic mice was lower than that of ICGN mice). In the histopathologic analysis of the kidney sections,congenic mice showed milder phenotypes than ICGN mice. These results confirmed the existence of the CKD-resistant/susceptible locus on Chr 2.
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Current Status of Research Progress |
Current Status of Research Progress
2: Research has progressed on the whole more than it was originally planned.
Reason
Progressing rather smoothly.
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Strategy for Future Research Activity |
We will find the presence of non-synonymous SNPs, and compare the expression profile of mRNA using microarray between both strains. We will select candidate genes and knock down theses genes in kidney cell lines.
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Causes of Carryover |
マウスが予想に反して繁殖しなかったためだが、現在はこの問題も解決した。
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Expenditure Plan for Carryover Budget |
マイクロアレイ、次世代シークエンサーなどの高額な解析を行い、全額使用する予定である。
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