| Budget Amount *help |
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2011: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2009: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2008: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
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| Research Abstract |
IgA nephropathy is characterized by mesangial deposition of IgA1 and galactose-deficient IgA1 is assumed to play a pathogenic role. However, the identity of the receptor for IgA1 is still controversial. Hence, the aim of this study was to explore the receptor for galactose-deficient IgA1. Human monoclonal IgA1 was treated with exoglycosidase and FITC-conjugated galactose-deficient IgA1 was used as a probe to detect the receptor in cultured human mesangial cells. According to comprehensive gene expression analysis, we revealed that galactose-deficient IgA1-collagen complex formation would be proposed as one of the candidate mechanisms of IgA1 deposition and proliferative signal transduction via integrinα2/β1 heterodimer in human mesangial cells.
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