2012 Fiscal Year Final Research Report
The development of the mechanism of inflammation regulation and the biomarker in IgA nephropathy with the use of glycomics
Project/Area Number |
23790943
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Kidney internal medicine
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Research Institution | Kyoto University |
Principal Investigator |
INOUE Tatsuyuki 京都大学, iPS 細胞研究所, 研究員 (60598564)
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Project Period (FY) |
2011 – 2012
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Keywords | 腎臓学 / IgA 腎症 |
Research Abstract |
We analyzed the mechanism of glomerular inflammation by the aberrantly glycosylated IgA. The expression of adiponectin was downregulated in cultured human glomerular cellsstimulated by the deglycosylated IgA, and was also in glomeruli in the patients of IgA nephropathy.We developed the methods of the aberrantly glycosylated IgA in patients with IgA nephropathy . The deglycosylated IgA in the renal tissue was certified by the staining of HA lectin. The urine deglycosylated IgA I was certified by the methods combined with two lectins, the urine deglycosylated IgA in the patients with IgA nephropathy was significantly increased compared with the other kidney disease.
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Research Products
(3 results)
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[Presentation] Aberrantly glycosylated IgA1 diminishes adiponectin expression in glomerular mesangial cells in vitro and in vivo: A novel anti-inflammatory mechanism in IgA nephropathy2011
Author(s)
Hitoshi Sugiyama, Tatsuyuki Inoue, Masashi Kitagawa, Keiichi Takiue, Hiroshi Morinaga, Yoko Kikumoto, Ayu Ogawa, Shinji Kitamura, Yohei Maeshima, Hirofumi Makino
Organizer
Kidney Week 2011, アメリカ腎臓学会
Place of Presentation
Philadelphia, USA.
Year and Date
2011-11-10
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