Article Sidebar
Published:
Jan 17, 2022Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
MiR-423-5p downregulates osteoblastic differentiation and cell viability by targeting SMAD3 in non-traumatic osteonecrosis
Abstract
Purpose: To investigate the potential role of miR-423-5p in osteoblastic differentiation of non-traumatic osteonecrosis of the femoral head (ONFH).
Methods: MiR-423-5p levels in bone marrow samples from ONFH and osteoarthritis (OA) patients, respectively, were evaluated using quantitative (real-time) polymerase chain reaction (qPCR). Osteoblastic differentiation was monitored using Alizarin red S staining, while cell viability was determined by MTT assay in hMSC-BM. MiR-423-5p expression was also measured during osteoblastic differentiation. The underlying mechanisms were explored using TargetScan database, and a series of in vitro experiments was performed to confirm this.
Results: MiR-423-5p levels were significantly upregulated in ONFH samples (p < 0.01) and miR-423-5p expression significantly increased in human mesenchymal stem cells-bone marrow (hMSC-BM) after bone morphogenetic protein 2 (BMP-2) treatment. Furthermore, miR-423-5p downregulated osteoblastic differentiation and suppressed cell viability. Furthermore, SMAD3 was observed to be a downstream target of miR-423-5p via bioinformatics analysis; further in vitro experiments confirmed this.
Conclusion: MiR-423-5p downregulates osteoblastic differentiation and cell viability by targeting SMAD3 in non-traumatic osteonecrosis. Thus, MiR-423-5p may serve as a potential target for promoting osteoblastic differentiation in ONFH patients.
