| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Research Abstract |
Glomerular visceral epithelial cells, also known as podocytes, serve as the final barrier to urinary protein loss. Podocyte injury may cause podocyte detachment, which leads to glomerulosclerosis. In our established model mice, severe podocyte injury induced podocyte loss and apoptosis, and glomeruloscrelosis. Using the mice model, we reported that treatment of 220oxa-calcitriol and Nothc2 agonist antibody suppressed podocyte loss and apoptosis. Furthermore, we reported that the measurement of urinary podocalyxin may be a useful biomarker to determine activity of IgA nephropathy and the effectiveness of corticosteroid treatment to IgA nephropathy.
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