2011 Fiscal Year Final Research Report

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
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
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.

(2 results)