| Project/Area Number |
26293201
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
後藤 眞 新潟大学, 医歯学系, 准教授 (00463969)
山本 卓 新潟大学, 医歯学総合病院, 准教授 (70444156)
金子 佳賢 新潟大学, 医歯学系, 講師 (80444157)
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| Co-Investigator(Renkei-kenkyūsha) |
YAMAMOTO Tadashi 新潟大学, 大学院医歯学総合研究科, 客員研究員 (30092737)
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| Research Collaborator |
YAMAGUCHI Hiroki
WATANABE Hirohumi
TUCHIDA Masahumi
CHO Takamasa
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥16,250,000 (Direct Cost: ¥12,500,000、Indirect Cost: ¥3,750,000)
Fiscal Year 2017: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2016: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2014: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
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| Keywords | IgA腎症 / ゲノム解析 / 家族性IgA腎症 / エクソーム解析 / メタゲノム解析 / プロテオミクス解析 / 糸球体腎炎 / エクソーム / メタゲノム / プロテオーム / エピゲノム / ゲノム / 口蓋扁桃 / マイクロバイオーム解析 / 扁桃 / 次世代シークエンサー |
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| Outline of Final Research Achievements |
To elucidate the etiology of IgA nephropathy, we tried to clarify the functional abnormality and disease process by analyzing simultaneously the host genomics, metagenomics of tonsils, and glomerular proteomics of samples from patients with IgAN. We observed the up-regulation of APRIL and production of galactose-deficient IgA1 (GdIgA1) in the tonsils, which was well correlated with the amount of deposition of GdIgA1 in the glomerulus. The possible involvement of periodontal anaerobic bacilli was suggested by IgA-Seq analysis of tonsils from the patients. The high activity of biosynthesis, TCA cycle, and carbon metabolism, whereas reduced activity of cytoskeleton structure of podocyte, were revealed by glomerular proteomics.
Genome analyses of both isolated and familial cases indicated that the abnormality in natural innate immunity and antigen presentation may be involved in the initiation of the IgA nephropathy.
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