We have located links that may give you full text access.
A potential therapeutic target for regulating osteoporosis via suppression of osteoclast differentiation.
Journal of Dentistry 2019 March
OBJECTIVES: Osteoclast differentiation is regulated by transcriptional, post-transcriptional and post-translational mechanisms. Micro-ribonucleic acids (miRNAs) are 20-24 nucleotides long non-coding RNAs involved in post-translational regulation of gene expressions during osteoclast differentiation. The objective of the present study was to investigate the role played by the miRNA, miR-338-3p, in osteoclastogenesis.
METHODS: Osteoclastogenesis was induced in murine RAW264.7 cells using M-CSF and RANKL. The differentiated cells were harvested at designated times for TRAP staining and detection of designated gene expressions. A synthetic miR-338-3p mimic or its inhibitor was transfected into RAW264.7 cells prior to the induction of osteoclastogenesis. The effects of mimic or inhibitor on osteoclastogenesis were examined by qRT-PCR and TRAP staining. Bioinformatic analysis and luciferase activity were performed to identify the relationship between miR-338-3p and the transcription factor MafB. The miR-338-3p mimic and MafB siRNA were co-transfected into RAW264.7 cells to evaluate the cross-talk between miR-338-3p and MafB.
RESULTS: miR-338-3p was increased significantly during osteoclast differentiation. Overexpression of miR-338-3p promoted osteoclastogenesis while its inhibition had the opposite effect. Bioinformatic analysis and dual luciferase assays indicated that miR-338-3p targeted MafB to repress its gene expression. MafB knockdown by RNA silencing blocked the promotional effect of miR-338-3p on osteoclast differentiation.
CONCLUSION: Because miR-338-3p is crucial for osteoclastic differentiation via targeting of the transcription factor MafB, inhibition of this miRNA represents a potential strategy for modulating osteoporosis in an aging population. CLINICAL SIGNIfiCANCE: Understanding the role played by miR-338-3p in osteoclast differentiation bridges the gap between the pathogenesis of osteoporosis and the quest for novel therapeutics to reduce the risk of bone fracture associated with this global disease.
METHODS: Osteoclastogenesis was induced in murine RAW264.7 cells using M-CSF and RANKL. The differentiated cells were harvested at designated times for TRAP staining and detection of designated gene expressions. A synthetic miR-338-3p mimic or its inhibitor was transfected into RAW264.7 cells prior to the induction of osteoclastogenesis. The effects of mimic or inhibitor on osteoclastogenesis were examined by qRT-PCR and TRAP staining. Bioinformatic analysis and luciferase activity were performed to identify the relationship between miR-338-3p and the transcription factor MafB. The miR-338-3p mimic and MafB siRNA were co-transfected into RAW264.7 cells to evaluate the cross-talk between miR-338-3p and MafB.
RESULTS: miR-338-3p was increased significantly during osteoclast differentiation. Overexpression of miR-338-3p promoted osteoclastogenesis while its inhibition had the opposite effect. Bioinformatic analysis and dual luciferase assays indicated that miR-338-3p targeted MafB to repress its gene expression. MafB knockdown by RNA silencing blocked the promotional effect of miR-338-3p on osteoclast differentiation.
CONCLUSION: Because miR-338-3p is crucial for osteoclastic differentiation via targeting of the transcription factor MafB, inhibition of this miRNA represents a potential strategy for modulating osteoporosis in an aging population. CLINICAL SIGNIfiCANCE: Understanding the role played by miR-338-3p in osteoclast differentiation bridges the gap between the pathogenesis of osteoporosis and the quest for novel therapeutics to reduce the risk of bone fracture associated with this global disease.
Full text links
Related Resources
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