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Advanced glycation end products increase expression of S100A8 and A9 via RAGE – MAPK in rat dental pulp cells
Author(s) -
Nakajima Y,
Inagaki Y,
Kido J,
Nagata T
Publication year - 2015
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.12280
Subject(s) - glycation , s100a9 , inflammation , pulp (tooth) , rage (emotion) , mapk/erk pathway , receptor , s100a8 , signal transduction , medicine , endocrinology , immunology , chemistry , biology , microbiology and biotechnology , dentistry , neuroscience
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. Materials and Methods Receptor for AGE ( RAGE ), S100A8, S100A9, and interleukin ( IL )‐1 β 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 ( PD 98059, SB 203580, and SP 60012) were used to investigate AGE signaling pathway. Results The mRNA levels of RAGE, S100A8, S100A9, and IL‐1 β were higher in diabetic pulp tissues. AGE increased mRNA expressions of S100A8, S100A9, and IL‐1 β 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‐1 β under diabetic pulp conditions, and AGE‐induced increases in S100A8 and S100A9 expressions may be associated with the RAGE–MAPK signaling pathway.