Novel mechanisms of pancreatic fibrosis and epithelial to mesenchymal transition in pancreatic diseases.
| Project/Area Number |
18590752
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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 |
Gastroenterology
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
SHIMIZU Kyoko Tokyo Women's Medical University, 医学部, 准教授 (90187451)
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| Project Period (FY) |
2006 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,230,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥630,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2007: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | 膵臓病学 / 膵星細胞 / 貪食作用 / 抗原提示細胞 / 獲得免疫 / MHC class II / HLA-DR / 線維化 / がん / 貪食 / 遺伝子発現 / 蛋白質 / 膵癌 / 膵炎 / 膵線維化 / 浸潤 / 増殖 / TGF-beta / 膵腺房細胞 / 貪食能 / 膵癌細胞株 / 浸潤能 / 遊走能 / 好中球 |
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| Research Abstract |
Pancreatic stellate cells (PSCs) play a pivotal role in pancreatic fibrogenesis in chronic pancreatitis and in the desmoplastic reaction in pancreatic cancer. We demonstrated that PSCs are associated with phagocytosis and innate immunity via toll-like receptors, but not with acquired immunity via MHC class II. PSCs that engulfed dead cells inhibited proliferation, invasion, and chemotaxis by pancreatic cancer cells in a manner that was mediated by luminal factors released by PSCs, suggesting that the phagocytic function of PSCs modulates the epithelial-mesenchymal transition in pancreatic cancer.
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Report
(6 results)
Research Products
(61 results)
