Interleukin-17A enhances osteogenic differentiation by activating ERK/MAPK in stem cells derived from human exfoliated deciduous teeth
DOI:
https://doi.org/10.15419/bmrat.v10i5.810Keywords:
Osteogenic differentiation, ERK/MAPK signalling pathway, stem cell, interleukin-17AAbstract
Introduction: Human exfoliated deciduous teeth?derived stem cells (SHEDs) have been shown as an excellent source of bone regeneration. Interleukin-17A (IL-17A) facilitates bone differentiation in various cell types, including SHEDs. In this study, we have demonstrated IL-17A?s stimulating effect on SHEDs in osteogenic differentiation and further evaluated the role of the ERK/MAPK signaling pathway in this process.
Methods: The function of IL-17A in osteogenic differentiation, proliferative activity, and MAPK cascade activation in SHEDs were investigated.
Results: IL-17A significantly enhanced proliferative and alkaline phosphatase activities in SHEDs. Furthermore, the expression levels of different osteogenic proteins including COL1A1, ALP, OPN, RUNX, and OCN were significantly elevated in IL-17A-treated SHEDs. Moreover, IL-17A triggered MAPK signaling in SHEDs, as evidenced by significant upregulation of both downstream ERK targets, P38 and JNK pathways, and upstream activators. In addition, ERK/MAPK activation time-dependently established the participation of MAPK signaling in SHED osteogenic differentiation.
Conclusion: These findings suggest that IL-17A-induced ERK/MAPK signaling pathway activation is necessary for SHEDs to differentiate into osteoblasts. This reiterates the significance of this particular intracellular signaling pathway in controlling SHED osteogenic differentiation, which is a promising source of bone tissue regeneration.
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Copyright The Author(s) 2017. This article is published with open access by BioMedPress. This article is distributed under the terms of the Creative Commons Attribution License (CC-BY 4.0) which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.