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Mitogen‐activated protein kinase/extracellular signal‐regulated protein kinase activation of cultured human dental pulp cells by low‐power gallium‐aluminium‐arsenic laser irradiation
Author(s) -
Miyata H.,
Genma T.,
Ohshima M.,
Yamaguchi Y.,
Hayashi M.,
Takeichi O.,
Ogiso B.,
Otsuka K.
Publication year - 2006
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/j.1365-2591.2006.01080.x
Subject(s) - mapk/erk pathway , kinase , protein kinase a , microbiology and biotechnology , p38 mitogen activated protein kinases , chemistry , biology
Aim To examine whether low‐power laser irradiation (LPLI) promotes cellular proliferation of human dental pulp‐derived fibroblast‐like cells (dental pulp cells). Methodology Dental pulp cells were obtained by primary culture of human dental pulp tissues from extracted third molar teeth. The phosphorylation of the mitogen‐activated protein kinase (MAPK) family after LPLI of these cells was investigated by Western blotting. By using a specific MAPK/ERK kinase (MEK) inhibitor (PD098059), the specific effect of LPLI on the MAPK pathway was also investigated by Western blotting as described above. The incorporation of [ 3 H]thymidine into the cells after LPLI was determined, and statistical analysis was performed by Wilcoxon signed‐ranks test. Results Extracellular signal‐regulated protein kinase (ERK) 1/2 was phosphorylated between 5 and 30 min after LPLI. Moreover, PD098059 inhibited LPLI‐mediated ERK1/2 activation. LPLI did not affect p38 MAPK or c‐Jun N‐terminal kinase (JNK) phosphorylation. But LPLI did not stimulate [ 3 H]thymidine incorporation into these cells. Conclusions These results indicated that LPLI activated MAPK/ERK, a signal for proliferation, differentiation and survival, but did not activate the stress signals p38 MAPK and JNK in human dental pulp cells.