Enterococcus faecalis attenuates osteogenesis through activation of p38 and ERK1/2 pathways in MC3T3‐E1 cells. (23rd December 2015)

• Record Type: Journal Article
• Authors: Wang, S.; Deng, Z.; Ye, X.; Geng, X.; Zhang, C.
• Is Part Of: International endontic journal. Volume 49:Number 12(2016:Dec.)
• Page Start: 1152
• Page End: 1164
• Publication Date: 2015-12-23
• Subjects: apoptosis -- differentiation -- Enterococcus faecalis -- MAPK signalling pathways -- mineralization -- osteoblasts; Endodontics -- Periodicals; 617.6342
• DOI: 10.1111/iej.12579
• Languages: English
• ISSNs: 0143-2885

Abstract

Abstract: Aim: To explore the role of Enterococcus faecalis in the proliferation, apoptosis and differentiation of osteoblasts. Methodology: Pre‐osteoblastic MC3T3‐E1 cells were treated with heat‐killed E. faecalis ATCC 29212 and clinical E. faecalis P25RC strains, respectively. Cell proliferation, mineralized calcium deposition, alkaline phosphatase (ALP) activity and apoptosis were assessed at various time‐points. The expression levels of osteogenic‐related genes including ALP, osteocalcin (OC), runt‐related protein 2 (Runx2) and collagen type 1 (COL1) were also analysed throughout the duration of the experiment. Additionally, the involvement of mitogen‐activated protein kinases (MAPKs) signalling pathways was analysed by Western blotting. In the presence of culture supernatant from E. faecalis ‐treated murine macrophages, apoptosis of MC3T3‐E1 cells was detected with flow cytometry. Data were analysed using analysis of variance (anova ), and P < 0.05 was considered significantly different. Results: E. faecalis significantly inhibited proliferation ( P < 0.05) and also significantly induced apoptosis of MC3T3‐E1 cells ( P < 0.05), whilst differentiation seemed to be unaffected after 7 days of E. faecalis treatment. However, osteogenic differentiation was significantly inhibited with 21‐day E. faecalis treatment ( P < 0.05). The p38 and ERK1/2 phosphorylation pathways associated with mineral deposition and apoptosis were significantly activated in MC3T3‐E1 cells. The culture supernatants from E. faecalis ‐treated macrophages induced osteoblast apoptosis. Conclusions: E. faecalis exerted an inhibitory effect on osteogenesis in pre‐osteoblastic MC3T3‐E1 cells via phosphorylation of p38 and ERK1/2.