Add like
Add dislike
Add to saved papers

FGF18 inhibits MC3T3‑E1 cell osteogenic differentiation via the ERK signaling pathway.

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.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

Related Resources

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app