| Project/Area Number |
22591175
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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 |
Pediatrics
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| Research Institution | Hirosaki University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IMAIZUMI Tadaatsu 弘前大学, 大学院・医学研究科, 教授 (90232602)
YOSHIDA Hidemi 弘前大学, 大学院・医学研究科, 講師 (40201008)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 小児腎 / 泌尿器科学 / 小児腎・泌尿器科学 / レチノイン酸誘導遺伝子アイ / Retinoic acid-inducible gene-I / polyinosinic-polycytidylic acid / 培養ヒトメサンギウム細胞 / Toll-like receptor 3 / Interferon stimulated gene 20 / 培養ヒトメサンギム細胞 / Toll-like receptor3 / CC chemokine ligand5 / interferon-β |
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| Research Abstract |
Viral infections may trigger the development of inflammatory renal disease or the worsening of pre-existing renal disease. Viral double-stranded RNA (dsRNA) can activate not only toll-like receptors (TLR) 3 located within intracellular endosomes and retinoic acid-inducible gene-I (RIG-I)-like helicase receptors located within the cytosol. RIG-I and melanoma differentiation-associated gene-5 (MDA5) are members of the RNA helicase family in the cytosol, and both act as pathogen recognition receptors. The activation of TLRs and their downstream immune responses can be induced by both infectious pathogens and non-infectious stimuli such as endogenous ligands, and this mechanism may be involved in the pathogenesis of autoimmune renal diseases. Based on our recent experimental studies using cultured normal human mesangial cells (MCs), we found that novel TLR3/RIG-I-mediated signaling pathways in MCs may be involved in the pathogenesis of glomerular diseases.
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