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IL-6 Induces Osteoblastic Differentiation of Periodontal Ligament Cells
K. Iwasaki1,
M. Komaki2,*,
K. Mimori1,
E. Leon1,
Y. Izumi1 and
I. Ishikawa3
1 Departments of Hard Tissue Engineering (Periodontology) and
2 Nanomedicine (DNP), Tokyo Medical and Dental University Graduate School, 1-5-45 Yushima, Bunkyoku, Tokyo 113-8549, Japan; and
3 Institute of Advanced Biomedical Engineering and Science, Tokyo Women’s Medical University, Japan
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Figure 1. IL-6/sIL-6R enhances ascorbic-acid-induced alkaline phosphatase activity in periodontal ligament cells. Periodontal ligament cells were stimulated with ascorbic acid (50 µg/mL), IL-6 (50 ng/mL), or sIL-6R (40 ng/mL) alone or in combination, as indicated. Alkaline phosphatase activity was examined by alkaline phosphatase staining (A) and alkaline phosphatase activity assay (B) (bar = 100 µm) 7 days after stimulation. *Significantly different from control (p < 0.05). **Significantly different from ascorbic acid (p < 0.001). Data in graphs are presented as the mean ± SD of 3 experiments.
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Figure 2. Effects of ascorbic acid, IL-6, and sIL-6R on Runx2 gene expression. Periodontal ligament cells were stimulated with ascorbic acid (50 µg/mL), IL-6 (50 ng/mL), or sIL-6R (40 ng/mL) alone or in combination, as indicated. Runx2 gene expression was examined by real-time PCR with cDNA from periodontal ligament cells at 3 and 6 days after stimulation. The expression levels of transcripts were compared with the level of an internal control (GAPDH). Three independent experiments were performed, and representative results are shown.
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Figure 3. Involvement of IGF-I in IL-6/sIL-6R-induced alkaline phosphatase activity. Periodontal ligament cells were stimulated with indicated combinations of IL-6 (50 ng/mL), sIL-6R (40 ng/mL), ascorbic acid (50 µg/mL), IGF-I (0.2–200 ng/mL), or anti-IGF-I antibody (40 or 80 µg/mL) for 7 days. Production of IGF-I was examined by enzyme-linked immunosorbent assay (A). Effect of exogenous IGF-I on alkaline phosphatase activity in periodontal ligament cells was investigated (B). Effect of IGF-I antibody on ascorbic acid+IL-6/sIL-6R-induced alkaline phosphatase activity in periodontal ligament cells was studied (C). *Significantly different from control (p < 0.05). **Significantly different from ascorbic acid (p < 0.001). ***Significantly different from ascorbic acid+IL-6/sIL-6R (p < 0.001). Data in graphs are presented as the mean ± SD of 3 experiments.
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Figure 4. Effects of MAPK and JAK/STAT inhibitors on alkaline phosphatase activity. PD98059 was used to inhibit ERK, and AG49 and JAK inhibitor I were used for JAK/STAT signaling inhibition. Periodontal ligament cells were pre-incubated with DMSO, PD98059 (20 µM), AG490 (AG, 20 µM), or JAK inhibitor I (JAK, 15 nM) for 30 min and cultured with or without ascorbic acid, IL-6, and sIL-6R for 7 days. We examined alkaline phosphatase staining (A,C) and alkaline phosphatase activity (B,D) (bar = 100 µm) to identify the effects of inhibitors of alkaline phosphatase activity on periodontal ligament cells. *Significantly different from ascorbic acid+IL-6/sIL-6R (p < 0.05). **Significantly different from ascorbic acid+IL-6/sIL-6R (p < 0.05). Data in graphs are presented as the mean ± SD of 3 experiments.
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Journal of Dental Research, Vol. 87, No. 10,
937-942 (2008)
DOI: 10.1177/154405910808701002
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