| Project/Area Number |
25430083
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | ICGNマウス / 慢性腎臓病 / ポドサイト / 尿細管間質傷害 / Tensin2 / podocyte / ICGN / ICGN mouse / chronic kidney disease / glomerulosclerosis / anemia / proteinuria |
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| Outline of Final Research Achievements |
Tensin2 (Tns2) deficiency results in alterations in podocytes and subsequent glomerular and tubulointerstitial injuries. However, this pathology is critically dependent on genetic background. While the Tns2-deficient podocytes of resistant murine strains, including C57BL/6J (B6) mice, remain almost intact, susceptible murine strains with Tns2 deficency, including ICGN mice, develop chronic kidney disease following alterations in the podocyte foot processes. Genome-wide linkage analysis was utilized to identify the QTL associated with the disease phenotypes on mouse chromosome (chr) 2. We developed 6 subcongenic strains that carry B6-derived chr segments from the consomic strain. One showed significantly milder albuminuria, another showed significantly milder tubulointerstitial injury. These data indicate that mouse chr 2 harbors two major genes associated with the severities of nephropathy induced by Tns2 deficiency.
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