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Regulation Mechanism of Osteoblast/Osteoclast Differentiation
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Regulation Mechanism of Osteoblast/Osteoclast Differentiation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 15 June 2024 | Viewed by 2283

Special Issue Editors

Prof. Dr. Hyung-Mun Yun

E-Mail Website
Guest Editor
Department of Oral Maxillofacial Pathology, School of Dentistry, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea
Interests: molecular and cellular pathology; 5-hydroxytryptamine; differentiation; regeneration; bone; CNS
Special Issues, Collections and Topics in MDPI journals
Dr. Kyung-Ran Park

E-Mail Website
Guest Editor
Korea Basic Science Institute (KBSI), Natural Science Campus, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul 02841, Republic of Korea
Interests: stem cell; differentiation; regeneration; bone development
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The differentiation of osteoblasts and osteoclasts plays a central role in bone formation and remodeling by tightly regulating bone matrix mineralization. Pathologically, impaired differentiation induces bone diseases such as osteoporosis and associated diseases such as cancer and metabolic diseases. Therefore, research targeting osteoblast or osteoclast differentiation is attracting attention as a promising strategy for the prevention and treatment of these diseases. This Special Issue focuses on the “Regulation Mechanism of Osteoblast/Osteoclast Differentiation”, contributing to bone development, formation, remodeling, and diseases through in vitro and/or in vivo studies. We warmly welcome submissions, including original papers and reviews, on this widely discussed topic.

Prof. Dr. Hyung-Mun Yun
Dr. Kyung-Ran Park
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bioactive compound
  • bone formation
  • bone remodeling
  • bone diseases
  • cancer
  • osteoblast
  • osteoclast

Published Papers (2 papers)

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Research

15 pages, 2683 KiB  
Article
Osteogenic Activities of Trifolirhizin as a Bioactive Compound for the Differentiation of Osteogenic Cells
by Hyung-Mun Yun, Mi Hyeon Cho, Hoibin Jeong, Soo Hyun Kim, Yun Hee Jeong and Kyung-Ran Park
Int. J. Mol. Sci. 2023, 24(23), 17103; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms242317103 - 04 Dec 2023
Viewed by 1079
Abstract
Plant extracts are widely used as traditional medicines. Sophora flavescens Aiton-derived natural compounds exert various beneficial effects, such as anti-inflammatory, anticancer, antioxidant, and antiregenerative activities, through their bioactive compounds, including flavonoids and alkaloids. In the present study, we investigated the biological effects of [...] Read more.
Plant extracts are widely used as traditional medicines. Sophora flavescens Aiton-derived natural compounds exert various beneficial effects, such as anti-inflammatory, anticancer, antioxidant, and antiregenerative activities, through their bioactive compounds, including flavonoids and alkaloids. In the present study, we investigated the biological effects of an S. flavescens-derived flavonoid, trifolirhizin (trifol), on the stimulation of osteogenic processes during osteoblast differentiation. Trifol (>98% purity) was successfully isolated from the root of S. flavescens and characterized. Trifol did not exhibit cellular toxicity in osteogenic cells, but promoted alkaline phosphatase (ALP) staining and activity, with enhanced expression of the osteoblast differentiation markers, including Alp, ColI, and Bsp. Trifol induced nuclear runt-related transcription factor 2 (RUNX2) expression during the differentiation of osteogenic cells, and concomitantly stimulated the major osteogenic signaling proteins, including GSK3β, β-catenin, and Smad1/5/8. Among the mitogen-activated protein kinases (MAPKs), Trifol activated JNK, but not ERK1/2 and p38. Trifol also increased the osteoblast-mediated bone-forming phenotypes, including transmigration, F-actin polymerization, and mineral apposition, during osteoblast differentiation. Overall, trifol exhibits bioactive activities related to osteogenic processes via differentiation, migration, and mineralization. Collectively, these results suggest that trifol may serve as an effective phytomedicine for bone diseases such as osteoporosis. Full article
(This article belongs to the Special Issue Regulation Mechanism of Osteoblast/Osteoclast Differentiation)
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14 pages, 1895 KiB  
Article
Impact of Mechanical Strain and Nicotinamide on RUNX2-Deficient Osteoblast Mimicking Cleidocranial Dysplasia
by Agnes Schröder, Talia Örs, Ye-Oun Byeon, Fabian Cieplik, Peter Proff, Christian Kirschneck and Eva Paddenberg
Int. J. Mol. Sci. 2023, 24(23), 16581; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms242316581 - 21 Nov 2023
Viewed by 724
Abstract
Cleidocranial dysplasia (CCD) is a rare genetic defect caused by a heterozygous mutation of runt-related transcription factor 2 (RUNX2), which is important for osteoblast and skeletal development. RUNX2-deficiency causes extra- and intra-oral malformations that often require orthodontic treatment. Nicotinamide (NAM) affects bone remodelling [...] Read more.
Cleidocranial dysplasia (CCD) is a rare genetic defect caused by a heterozygous mutation of runt-related transcription factor 2 (RUNX2), which is important for osteoblast and skeletal development. RUNX2-deficiency causes extra- and intra-oral malformations that often require orthodontic treatment. Nicotinamide (NAM) affects bone remodelling processes. As these are crucial for orthodontic therapy, NAM could improve orthodontic treatment in CCD patients. This study investigates the effect of NAM in control and RUNX2-deficient osteoblasts under mechanical strain mimicking orthodontic treatment. First, the optimal NAM concentration and the differences in the expression profile of control and RUNX2-deficient osteoblasts were determined. Subsequently, osteoblasts were exposed to tensile and compressive strain with and without NAM, and the expression of genes critically involved in bone remodelling was investigated. NAM increased the expression of bone remodelling genes. RUNX2-deficient osteoblasts expressed more receptor activator of NFkB ligand (RANKL) and interleukin-6 (IL6), but less colony-stimulating factor-1 (CSF1). Most of the positive effects of NAM on bone remodelling genes were impaired by mechanical loading. In conclusion, NAM stimulated osteoblast differentiation by increasing the expression of RUNX2 and regulated the expression of osteoclastogenic factors. However, the positive effects of NAM on bone metabolism were impaired by mechanical loading and RUNX2 deficiency. Full article
(This article belongs to the Special Issue Regulation Mechanism of Osteoblast/Osteoclast Differentiation)
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