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S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells
Joint Authors
Yumoto, Hiromichi
Takagi, Ryosuke
Sakamoto, Eijiro
Kido, Jun-ichi
Inagaki, Yuji
Hiroshima, Yuka
Naruishi, Koji
Source
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-02-20
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Objective.
Calprotectin is a heterocomplex of S100A8 and S100A9 and is mainly secreted from neutrophils, monocytes, and chondrocytes in inflammatory condition.
Calprotectin binds to RAGE and TLR4 and induces the expression of proinflammatory chemokines and cytokines in various cells.
Periodontitis is a chronic inflammatory disease that leads to gingival inflammation and alveolar bone resorption.
Calprotectin levels in gingival crevicular fluid of periodontitis patients are higher than healthy patients.
In the present study, the effects of S100A8 and S100A9 on the expressions of proinflammatory cytokines and bone metabolism-related factors in mouse osteocyte-like cells (MLO-Y4-A2) were investigated.
Design.
MLO-Y4-A2 cells were treated with S100A8 and S100A9, and the expressions of RAGE, TLR4, RANKL, and several inflammatory cytokines were analyzed by PCR and Western blotting or ELISA methods.
To investigate the intracellular signaling pathways, phosphorylation of MAPK and STAT3 was determined by Western blotting, and chemical specific inhibitors and siRNAs were used.
Results.
Expressions of IL-6 and RANKL were increased by treatment with S100A9 but not S100A8.
However, both S100A8 and S100A9 did not change expression of IL-1β, IL-8, and TNF-α.
Although RAGE and TLR4 expressions were not upregulated by S100A9 treatment, transfection of siRNA for RAGE and TLR4 significantly decreased IL-6 and RANKL expressions.
In addition, S100A9 activated p38, ERK, and STAT3 signaling pathways, and inhibitors for these factors significantly decreased S100A9-induced IL-6 and RANKL expressions.
Conclusions.
These results indicated that S100A9 induces IL-6 and RANKL production via engagement with RAGE and TLR4 signalings in osteocytes and suggested that S100A9 may play important roles in the periodontal alveolar bone destruction.
American Psychological Association (APA)
Takagi, Ryosuke& Sakamoto, Eijiro& Kido, Jun-ichi& Inagaki, Yuji& Hiroshima, Yuka& Naruishi, Koji…[et al.]. 2020. S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells. BioMed Research International،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1136591
Modern Language Association (MLA)
Takagi, Ryosuke…[et al.]. S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells. BioMed Research International No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1136591
American Medical Association (AMA)
Takagi, Ryosuke& Sakamoto, Eijiro& Kido, Jun-ichi& Inagaki, Yuji& Hiroshima, Yuka& Naruishi, Koji…[et al.]. S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1136591
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1136591