title: Advanced glycation end products increase expression of S100A8 and A9 via RAGE-MAPK in rat dental pulp cells.
abstract: OBJECTIVE
  Advanced glycation end products (AGE) are involved in the progression of diabetic complications. Although our previous reports show that AGE increased dental pulp calcification, AGE accumulation is also associated with inflammation. This study examined AGE effect on the expression of inflammation factors using rat dental pulp tissues and cell cultures.
  
  
  METHODS
  Receptor for AGE (RAGE), S100A8, S100A9, and interleukin (IL)-1β were selected as inflammation parameters. Rat dental pulp cells were cultured and treated with AGE, and the effects were determined by real-time PCR. An anti-RAGE antibody or MAPK pathway inhibitors (PD98059, SB203580, and SP60012) were used to investigate AGE signaling pathway.
  
  
  RESULTS
  The mRNA levels of RAGE, S100A8, S100A9, and IL-1β were higher in diabetic pulp tissues. AGE increased mRNA expressions of S100A8, S100A9, and IL-1β in cultured dental pulp cells. In the presence of anti-RAGE antibody, AGE did not increase in S100A8 or S100A9 expressions. The AGE-induced increases in S100A8 and S100A9 were inhibited by PD98059 and SB203580, respectively.
  
  
  CONCLUSIONS
  Advanced glycation end products increased mRNA expression of S100A8, S100A9, and IL-1β under diabetic pulp conditions, and AGE-induced increases in S100A8 and S100A9 expressions may be associated with the RAGE-MAPK signaling pathway.
authors.affiliation: Department of Periodontology and Endodontology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Nakajima
authors.forename: Y
authors.initials: Y
authors.lastname: Inagaki
authors.forename: J
authors.initials: J
authors.lastname: Kido
authors.forename: T
authors.initials: T
authors.lastname: Nagata
mesh_terms: D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D040501:Calgranulin A / Q000235:genetics / Q000378:metabolism*; D040502:Calgranulin B / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D003782:Dental Pulp / Q000166:cytology / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000378:metabolism*; D005419:Flavonoids / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects; D017127:Glycation End Products, Advanced / Q000494:pharmacology*; D007093:Imidazoles / Q000494:pharmacology; D053583:Interleukin-1beta / Q000235:genetics; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D000067759:Receptor for Advanced Glycation End Products / Q000235:genetics / Q000276:immunology / Q000378:metabolism
chemical_list: C000593874:Ager protein, rat; D000906:Antibodies; D040501:Calgranulin A; D040502:Calgranulin B; D005419:Flavonoids; D017127:Glycation End Products, Advanced; D007093:Imidazoles; D053583:Interleukin-1beta; D011725:Pyridines; D012333:RNA, Messenger; D000067759:Receptor for Advanced Glycation End Products; D020928:Mitogen-Activated Protein Kinases; C093642:SB 203580; C093973:2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one
keywords: RAGE-MAPK signaling; S100A8; S100A9; advanced glycation end products; dental pulp; diabetes