2022 Fiscal Year Final Research Report
Mechanism of the glomerular injury after IgA deposition on mesangial cells in IgA nephropathy model mice
| Project/Area Number |
20K08588
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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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| Review Section |
Basic Section 53040:Nephrology-related
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| Research Institution | Niigata University |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Keywords | IgA腎症 |
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| Outline of Final Research Achievements |
IgA nephropathy is a primary glomerulonephritis characterized by deposition of IgA1 in the glomerular mesangial region. Gene transfer by intravenous administration of the B cell activation factor of the TNF family (BAFF)-gene expression vector into mice induced elevated level of serum IgA and deposition of IgA in the renal glomerular mesangial region. Mesangial cell hyperplasia and mesangial matrix increase were observed 12 months later, and severe glomerular injuries such as mesangial lysis were demonstrated 15 months later. As a result of comparing the expressed genes over time using RNA extracted from isolated glomeruli, gene X was identified as one of the genes whose expression was commonly increased after Baff gene transfer.
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| Free Research Field |
腎臓内科学
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| Academic Significance and Societal Importance of the Research Achievements |
IgA腎症は最も頻度の高い原発性糸球体腎炎であり、発症後約20～30年で20％から50％の患者に腎機能低下を認め、末期腎不全に至る主要な原疾患のひとつである。メサンギウム領域にIgA1が沈着する現象は同じでありながら、患者個々により組織学的重症度、臨床学的重症度は大きく異なり、腎予後に大きな差が生じる。経時的、網羅的解析により、糸球体障害進展の鍵となる分子が新たに同定されることにより、ヒト腎生検組織における新たな予後予測因子が確立することが期待される。
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