We have located links that may give you full text access.
Force-induced decline of FOXM1 in human periodontal ligament cells contributes to osteoclast differentiation.
Angle Orthodontist 2019 March 29
OBJECTIVES:: To investigate whether Forkhead family transcription factors are responsive to mechanical force and the resulting influence on the osteoclast differentiation mediated by human periodontal ligament cells (PDLCs).
MATERIALS AND METHODS:: A high-throughput RNA sequencing assay was performed in compressive force-stimulated and control human PDLCs. Alteration of FOXM1, a member of the Forkhead family transcription factors, was further confirmed by Western blotting and quantitative reverse-transcription polymerase chain reaction. Expression of FOXM1 was inhibited by either small interfering RNA (siRNA) transfection or addition of its specific inhibitor Siomycin A. Then, cells were exposed to compressive force and co-cultured with the murine macrophage cell line Raw264.7, followed by tartrate-resistant acid phosphatase staining assay. Expression changes of receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegetin (OPG) caused by FOXM1 suppression were measured. Alkaline phosphatase (ALP) staining, ALP activity assay, and crystal violet staining assay were performed after FOXM1 inhibition.
RESULTS:: FOXM1 transcription decreased after mechanical stimulation in PDLCs. Inhibition of FOXM1 promoted force-induced osteoclast differentiation of RAW264.7 and upregulated the RANKL/OPG ratio in PDLCs. Interference of FOXM1 led to promoted osteogenic differentiation but decreased proliferation of PDLCs.
CONCLUSIONS:: FOXM1 is a novel mechano-responsive gene in human PDLCs. Suppressing FOXM1 expression could promote osteoclast differentiation as well as RANKL/OPG in human PDLCs. FOXM1 also plays a role in controlling PDLC differentiation and proliferation capacity.
MATERIALS AND METHODS:: A high-throughput RNA sequencing assay was performed in compressive force-stimulated and control human PDLCs. Alteration of FOXM1, a member of the Forkhead family transcription factors, was further confirmed by Western blotting and quantitative reverse-transcription polymerase chain reaction. Expression of FOXM1 was inhibited by either small interfering RNA (siRNA) transfection or addition of its specific inhibitor Siomycin A. Then, cells were exposed to compressive force and co-cultured with the murine macrophage cell line Raw264.7, followed by tartrate-resistant acid phosphatase staining assay. Expression changes of receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegetin (OPG) caused by FOXM1 suppression were measured. Alkaline phosphatase (ALP) staining, ALP activity assay, and crystal violet staining assay were performed after FOXM1 inhibition.
RESULTS:: FOXM1 transcription decreased after mechanical stimulation in PDLCs. Inhibition of FOXM1 promoted force-induced osteoclast differentiation of RAW264.7 and upregulated the RANKL/OPG ratio in PDLCs. Interference of FOXM1 led to promoted osteogenic differentiation but decreased proliferation of PDLCs.
CONCLUSIONS:: FOXM1 is a novel mechano-responsive gene in human PDLCs. Suppressing FOXM1 expression could promote osteoclast differentiation as well as RANKL/OPG in human PDLCs. FOXM1 also plays a role in controlling PDLC differentiation and proliferation capacity.
Full text links
Related Resources
Trending Papers
Proximal versus distal diuretics in congestive heart failure.Nephrology, Dialysis, Transplantation 2024 Februrary 30
World Health Organization and International Consensus Classification of eosinophilic disorders: 2024 update on diagnosis, risk stratification, and management.American Journal of Hematology 2024 March 30
Heart failure with preserved ejection fraction: diagnosis, risk assessment, and treatment.Clinical Research in Cardiology : Official Journal of the German Cardiac Society 2024 April 12
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
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