Cellular response in preventing or inducing atherosclerosis
| Project/Area Number |
20500400
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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 |
Biomedical engineering/Biological material science
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| Research Institution | Nihon University |
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Principal Investigator |
MITSUMATA Masako Nihon University, 医学部, 教授 (40064589)
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| Co-Investigator(Kenkyū-buntansha) |
ESUMI Mariko 日本大学, 医学部, 准教授 (30167291)
KUSUMI Yoshiaki 日本大学, 医学部, 講師 (60186393)
ABIKO Yoshimitsu 日本大学, 松戸歯学部, 教授 (70050086)
江角 眞理子 日本大学, 医学部, 准教授 (10147019)
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| Co-Investigator(Renkei-kenkyūsha) |
AZUMA Kousuke 順天堂大学, 医学部, 助手 (40420830)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 粥状硬化 / 内皮細胞 / 増殖 / 単球接着 / p21^<sdi / cip / waf1> / thioredoxin interacting protein / Porphyromonas gingivalis / Toll-like receptor (TLR)2 / ヒト粥状硬化 / 歯周病菌 / r40(HBP35)蛋白 / マクロファージ / 歯周病菌リポ蛋白(LPS) / サイトカイン / ずり応力 / p21 / TXNIP / apoptosis / 酸化 / chemokines |
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| Research Abstract |
1. We examined the role of p21^<Sdi/Cip/Waf1> (p21), a growth inhibitor induced by laminar shear stress (LS), in monocyte adhesion to endothelial cells (ECs). Both EC proliferation and monocyte adhesion induced by disturbed shear stress (DS) were inhibited by p21-overexpression. p21-overexpression significantly suppressed the DS-induced expression of thioredoxin interacting protein, vascular cell adhesion molecule and chemokines, indicating that p21 may function to prevent atherogenesis by regulating the redox balance, which leads to the inhibition of adhesion molecule expression in ECs under LS. 2. Porphyromonas gingivalis (Pg) protein (Pg-r40kDa) was detected mainly in macrophages in 72-82% of human aortic atheromas, but not Fatty streak, DIT and coronary atheromas. Conditioned medium from macrophages stimulated with Pg-LPS induced the expression of TLR2 mRNA in ECs, indicating that Pg induces atherosclerosis, regulating the inflammatory cross talk between ECs and macrophages
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Report
(4 results)
Research Products
(23 results)
