Elucidate of deteriorating mechanism of diabetic and periodontitis via receptor of advanced glycation endproducts

Research Project

Project/Area Number	22792088
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Periodontal dentistry
Research Institution	Hiroshima University
Principal Investigator	UCHIDA Yushi 広島大学, 大学院・医歯薬学総合研究科, 助教 (40363080)
Project Period (FY)	2010 – 2011
Project Status	Completed (Fiscal Year 2011)
Budget Amount *help	¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000) Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000) Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords	S100タンパク質 / 歯肉上皮細胞 / 歯肉線維芽細胞 / IL-8 / 細胞間コミュニケーション / connexin43 / 骨髄由来間葉系幹細胞 / 石灰化能 / 糖尿病 / 歯周病 / 糖最終産物 / S100 / 歯肉繊維芽細胞
Research Abstract	S100 protein increased the IL-8 levels in HGEC. Amounts of IL-8 in HGEC stimulated by S100 protein were 1. 5 times higher than non-stimulated cells for 48 hours. Production of connexin43 in HGEC was induced by 1. g/ ml S100 protein for 6 hours. However, production of connexin43 declined in HGEC stimulated by 10. g/ ml S100 protein for 24 hours. Gap junctional intercellular communication was induced by 1. g/ ml S100 protein for 12 hours, but inhibited by 10. g/ ml S100 protein for 24 hours. Porphynomonas gingivalis might induce IL-8 in HGEC via Receptor of advanced glycation endproducts.

Report

(3 results)