| Project/Area Number |
23592662
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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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| Research Field |
Plastic surgery
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| Research Institution | Kurume University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Misa 山口大学, 大学院医学系研究科, 講師 (70379957)
KIYOKAWA Kensuke 久留米大学, 医学部, 教授 (10195399)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 良性腫瘍 / 発生・分化 / 細胞・組織 / 遺伝子 / 病理学 |
|---|
| Research Abstract |
Neurofibromas are benign tumors that comprise primarily of Schwann cells and fibroblasts. Mast cells have been found scattered in the tumor tissue, and their role in promoting the proliferation of neurofibroma has been suggested. We have clarified that mast cells significantly promoted proliferation of the NF1 cells and upper the levels of TGFb1, SCF and MnSOD. In this study, we observed association between MnSOD and its transcription factor Nuclear factor kappa B. We clarified that NFkB-p65, phospho-IkB, phospho-p65 in co-culture of NF1 cells and mast cells using western blotting. MnSOD was later than the other protein expression. MnSOD in the NF1 cells were increased after LPS stimulation and strongly decreased after tranilast (anti-allergic agent) and BAY11-7082 (NFkB inhibitor) stimulations compared without them. Hence, these results suggest a possibility that soluble factor involved in the cell-cell interaction activates NFkB signaling pathway for transcription of MnSOD.
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