کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3148177 | 1197390 | 2015 | 6 صفحه PDF | دانلود رایگان |
• Effect of LPS on mineralization in odontoblast-like cells.
• Involvement of TLR4 signaling in the effects of LPS on OLCs.
• Involvement of MAPK signaling in the effects of LPS on OLCs.
• Involvement of PI3K/Akt signaling in the effects of LPS on OLCs.
IntroductionOdontoblasts play an important role in post-developmental control of mineralization in response to external stimuli in the tooth. The present study investigated whether lipopolysaccharide (LPS), a major bacterial cell wall component, influenced mineralization in a murine odontoblast-like cell (OLC) line and the related intracellular signaling pathways involved.MethodsAlizarin red S staining was used to assess mineralized nodule formation in OLCs in response to LPS. The effects of LPS on gene expression of odontoblastic markers were investigated by using quantitative real-time reverse-transcriptase polymerase chain reaction. The potential involvement of toll-like receptor 4 (TLR4), nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), or phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways in the mineralized nodule formation, and mRNA expression of several odontoblastic markers of OLCs induced by LPS was assessed by using alizarin red S staining and quantitative real-time reverse-transcriptase polymerase chain reaction. Moreover, LPS stimulation resulted in phosphorylation of protein that was determined by Western blot analysis.ResultsOLCs showed reduced mineralized nodule formation and several odontoblastic markers expression in response to LPS exposure. Furthermore, inhibition of TLR4, extracellular signal-regulated kinase (ERK), and PI3K/Akt signaling noticeably antagonized LPS-mediated mineralization in OLCs. However, p38 MAPK, c-Jun N-terminal kinase, and NF-κB signaling inhibitors did not affect LPS-mediated mineralization in OLCs. Notably, LPS treatment resulted in a time-dependent phosphorylation of ERK and PI3K/Akt in OLCs, which was abrogated by their specific inhibitors.ConclusionsLPS decreased mineralization in OLCs via TLR4, ERK MAPK, and PI3K/Akt signaling pathways, but not p38, c-Jun N-terminal kinase, or NF-κB signaling.
Journal: Journal of Endodontics - Volume 41, Issue 6, June 2015, Pages 871–876