| Project/Area Number |
21591032
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | The University of Tokushima |
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Principal Investigator |
MATSUURA Motokazu (2010-2011) 徳島大学, 病院, 医員 (10403734)
村上 太一 (2009) The University of Tokushima, 大学院・ヘルスバイオサイエンス研究部, 助教 (30403736)
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| Co-Investigator(Kenkyū-buntansha) |
TOMINAGA Tatsuya 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教 (80425446)
松浦 元一 徳島大学, 医学部・歯学部附属病院, 医員 (10403734)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 糸球体腎炎 / 糖膜蛋白 / ポドサイト / Tpbg / アクチン骨格 / TGFβ / 抗体治療 / TGF-β |
|---|
| Research Abstract |
Trophoblast glycoprotein(Tpbg) is one of a single pass transmembrane glycoproteins. Differentiated podocytes expresses abundant stress fiber. Tpbg was colocalized with the focal adhesion(FA) protein, Vinculin, along with stress fiber formation by immunofluorescence. Tpbg localization at the FA was induced by dominant-active RhoA in undifferentiated podocyte, and suppressed by ROCK inhibitor. In addition, TGF-βenhanced Tpbg assembly at the FA in parallel with rearrangement of stress fibers. Tpbg was upregulated in injured podocytes in accordance with the mesangial proliferation of Thy1 GN. These results suggest that Tpbg is involved in phenotypic alteration of injured podocytes by modulating actin cytoskeleton in glomerulonephritis.
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