2005 Fiscal Year Final Research Report Summary
Analysis for pathogenesis of lipoprotein glomerulopathy using apoE/Fc receptor γ chain double deficient mouse
| Project/Area Number |
16590806
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | FUKUOKA UNIVERSITY |
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Principal Investigator |
SAITO Takao FUKUOKA UNIVERSITY, FACULTY OF MEDICINE, PROFESSOR, 医学部, 教授 (10125552)
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| Co-Investigator(Kenkyū-buntansha) |
SAKU Keijiro FUKUOKA UNIVERSITY, FACULTY OF MEDICINE, PROFESSOR, 医学部, 教授 (40183371)
KANEOKA Hidetoshi FUKUOKA UNIVERSITY, HOSPITAL, ASSOCIATE PROFESSOR, 病院・助教授 (20161169)
OGAHARA Satoru FUKUOKA UNIVERSITY, HOSPITAL, ASSISTANT PROFESSOR, 病院・講師 (40233407)
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| Project Period (FY) |
2004 – 2005
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| Keywords | ApoE / FcRγ double deficient mouse / FcRγ deficient mouse / ApoE deficient mouse / Lipoprotein glomerulopathy / GVH reaction / Apolipoprotein E |
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| Research Abstract |
1.The breeding and propagation of apolipoprotein E (apoE)/FcR gamma-chain (FcRg) double deficient mice : An apoE/FcRg hetero deficient mouse (F1) was bred by the cross of an apoE deficient mouse and FcRg deficient mouse, and thereafter, a F2 mouse was obtained by the cross of F1 mice. ApoE/FcRg double deficient mice were confirmed in F2 mice by the genetic type in PCR and the Western blotting for apoE.
2.Induction of chronic graft versus host disease (cGVHD) in wild, FcRg deficient, apoE deficient and apoE/FcRg double deficient mice : The spleen-cell floating liquid extracted from the donor mouse B6.C-H2^<bm12> was injected via caudal-vein into wild, FcRg deficient, apoE deficient and apoE/FcRg double deficient mice of C57BL/6 strain to induce cGVHD.. The laboratory data and renal histology were compared with those of control mice at the same age in which spleen cells were not injected.
In the glomeruli of a few FcRg deficient mice, LPG-like lesions with typical lipoprotein thrombi were observed regardless of whether cGVHD was induced or not. On the other hand, cGVHD induced-apoE deficient mice showed prominent proliferation in the glomeruli. In addition, apoE/FcRg double deficient mice were not conspicuous by these changes but rather by glomerulosclerosis.
Therefore, it is suggested that the FcRg and apoE have a suppressive role in LPG and glomerulonephritis, respectively. These results must be useful for elucidating the mechanism of renal diseases.
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