Open AccessFGF18 inhibits MC3T3-E1 cell osteogenic differentiation via the ERK signaling pathway
Author(s) -
Feng Zhai,
Na Song,
Jian Ma,
Weiyue Gong,
Haishan Tian,
Xiaokun Li,
Chao Jiang,
Haijun Wang
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.7088
Subject(s) - alkaline phosphatase , osteocalcin , osteoblast , chemistry , fibroblast growth factor , microbiology and biotechnology , signal transduction , cellular differentiation , transcription factor , cell growth , biology , biochemistry , gene , receptor , enzyme , in vitro
Fibroblast growth factor (FGF) 18 is a member of the FGF family and serves a key role in skeletal growth and development. The present study investigated the effect of FGF18 on pre‑osteoblast MC3T3-E1 cells and the signaling pathways involved by performing an alkaline phosphatase (ALP) assay and reverse transcription‑quantitative polymerase chain reaction. MC3T3‑E1 cells incubated in a culture medium supplemented with FGF18 exhibited increased viability when compared with the untreated control cells. In addition, ALP activity was decreased in MC3T3‑E1 cells treated with FGF18 plus an osteogenic medium (OM) for 7 and 14 days when compared with untreated and OM‑treated controls. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) results demonstrated that the expression of osteoblastic‑associated genes was significantly repressed in FGF18 plus OM‑treated MC3T3‑E1 cells, including ALP, collagen type I, osteocalcin, bone sialo protein and osterix. These results suggested that the expression levels of genes associated with osteogenesis were mainly repressed. In addition, combined treatment of MC3T3‑E1 cells with OM and FGF18 led to a significant reduction in mineral deposition when compared with the OM‑only treated group. Furthermore, FGF18 activated the extracellular signal‑regulated kinase pathway in MC3T3‑E1 cells, which may have been responsible for the observed decrease in the expression of osteoblastic‑associated genes. In conclusion, the results suggest that FGF18 may be involved in MC3T3‑E1 cell proliferation and osteoblastic differentiation.