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Molecular Studies of Bone Biology and Bone Tissue
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Molecular Studies of Bone Biology and Bone Tissue

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: 20 December 2024 | Viewed by 4475

Special Issue Editor

Prof. Dr. Giovanna Iezzi

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Guest Editor
Department of Medical, Oral and Biotechnological Sciences, University of Chieti-Pescara, Chieti, Italy
Interests: biomaterials; bone regeneration; bioengineering; biomedical engineering
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue focuses on physiological mechanisms of bone biology and bone tissue. Bone is a crucial tissue involved in a variety of metabolic tasks, including body support, organ protection, mineral deposit, and hematological functions. It has recently been shown that bone tissue has endocrine functions, releasing hormonally active compounds, such as osteocalcin. Bone tissue is constantly rebuilt via the bone remodeling process which involves osteoclast-mediated bone resorption, followed by osteoblast-mediated bone synthesis. The discovery of processes underlying the pathophysiology of metabolic bone disorders continues to be a major research focus, drawing experts from all medical fields. Furthermore, biomaterial-mediated immune responses regulate fundamental bone processes, such as osteogenesis, osteoclastogenesis, and inflammation, demonstrating the importance in biomedical applications.

This Special Issue, “Molecular Studies of Bone Biology and Bone Tissue”, aims to provide new knowledge on the regulatory mechanisms of bone regeneration by focusing on the biological interplay between stem cell differentiation, the immune system, and the involvement of novel materials.

Authors are invited to submit original research and review articles related to these topics.

Potential topics include the following:

  • mechanisms of bone regeneration;
  • innovative materials for bone regeneration;
  • future bone tissue engineering applications;
  • pathophysiology of metabolic bone diseases;
  • role and use of stem cells in bone regeneration and repair;
  • crosstalk between bone cells and immune cells;
  • endocrine activities of bone tissue.

We welcome submissions of original articles, reviews, and communication. This Special Issue is supervised by Prof. Giovanna Iezzi, who is assisted by our Topical Advisory Panel Member: Dr. Emira D’Amico and Dr. Tania Vanessa Pierfelice (University of Chieti-Pescara).

Prof. Dr. Giovanna Iezzi
Guest Editor

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

  • bone
  • stem cells
  • immunomodulation
  • biomaterials
  • bone regeneration
  • bone repair
  • bone diseases

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Published Papers (4 papers)

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Research

13 pages, 1886 KiB  
Article
Hypomethylation of the RUNX2 Gene Is a New Potential Biomarker of Primary Osteoporosis in Men and Women
by Bulat Yalaev, Anton Tyurin, Karina Akhiiarova and Rita Khusainova
Int. J. Mol. Sci. 2024, 25(13), 7312; https://doi.org/10.3390/ijms25137312 - 3 Jul 2024
Viewed by 806
Abstract
The search for the molecular markers of osteoporosis (OP), based on the analysis of differential deoxyribonucleic acid (DNA) methylation in bone cells and peripheral blood cells, is promising for developments in the field of the early diagnosis and targeted therapy of the disease. [...] Read more.
The search for the molecular markers of osteoporosis (OP), based on the analysis of differential deoxyribonucleic acid (DNA) methylation in bone cells and peripheral blood cells, is promising for developments in the field of the early diagnosis and targeted therapy of the disease. The Runt-related transcription factor 2 (RUNX2) gene is one of the key genes of bone metabolism, which is of interest in the search for epigenetic signatures and aberrations associated with the risk of developing OP. Based on pyrosequencing, the analysis of the RUNX2 methylation profile from a pool of peripheral blood cells in men and women over 50 years of age of Russian ethnicity from the Volga-Ural region of Russia was carried out. The level of DNA methylation in three CpG sites of the RUNX2 gene was assessed and statistically significant hypomethylation was revealed in all three studied CpG sites in men (U = 746.5, p = 0.004; U = 784, p = 0.01; U = 788.5, p = 0.01, respectively) and in one CpG site in women (U = 537, p = 0.03) with primary OP compared with control. In the general sample, associations were preserved for the first CpG site (U = 2561, p = 0.0001766). The results were obtained for the first time and indicate the existence of potentially new epigenetic signatures of RUNX2 in individuals with OP. Full article
(This article belongs to the Special Issue Molecular Studies of Bone Biology and Bone Tissue)
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13 pages, 2542 KiB  
Article
Contribution of Osteoblast and Osteoclast Supernatants to Bone Formation: Determination Using a Novel Microfluidic Chip
by Sin Hyung Park, Hyun-Ju An, Haeri Kim, Insun Song and Soonchul Lee
Int. J. Mol. Sci. 2024, 25(12), 6605; https://doi.org/10.3390/ijms25126605 - 15 Jun 2024
Viewed by 606
Abstract
We fabricated a microfluidic chip (osteoblast [OB]–osteoclast [OC] chip) that could regulate the mixture amounts of OB and OC supernatants to investigate the effect of different supernatant distributions on osteogenesis or osteoclastogenesis. Computer-aided design was used to produce an OB–OC chip from polydimethylsiloxane. [...] Read more.
We fabricated a microfluidic chip (osteoblast [OB]–osteoclast [OC] chip) that could regulate the mixture amounts of OB and OC supernatants to investigate the effect of different supernatant distributions on osteogenesis or osteoclastogenesis. Computer-aided design was used to produce an OB–OC chip from polydimethylsiloxane. A pressure controller was assembled and different blends of OB and OC supernatants were correctly determined. OB and OC supernatants were placed on the upper panels of the OB–OC chip after differentiation for an in vitro evaluation. We then tested the changes in osteogenesis using MC3T3-E1 cells in the middle chambers. We observed that a 75:25 distribution of OB and OC supernatants was the most potent in osteogenesis. We then primed the osteogenic differentiation of MC3T3-E1 cells using an OB–OC mixed supernatant or an OB supernatant alone (supernatant ratios of 75:25 or 100:0, respectively). These cells were placed on the calvarial defect sites of rats. Microcomputed tomography and histological analyses determined a significantly higher bone formation in the group exposed to the OB–OC supernatant at a ratio of 75:25. In this study, we demonstrate the applicability of an OB–OC chip to evaluate the effect of different supernatant distributions of OB and OC. We observed that the highest bone-forming potential was in MC3T3-E1 cells treated with conditioned media, specifically the OB–OC supernatant at a ratio of 75:25. Full article
(This article belongs to the Special Issue Molecular Studies of Bone Biology and Bone Tissue)
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20 pages, 7534 KiB  
Article
Differential Gene Expression Involved in Bone Turnover of Mice Expressing Constitutively Active TGFβ Receptor Type I
by Ohnmar Myint, Nithidol Sakunrangsit, Jatuphol Pholtaisong, Parichart Toejing, Pinyada Pho-on, Asada Leelahavanichkul, Somyoth Sridurongrit, Chatchawit Aporntewan, Matthew B. Greenblatt and Sutada Lotinun
Int. J. Mol. Sci. 2024, 25(11), 5829; https://doi.org/10.3390/ijms25115829 - 27 May 2024
Cited by 1 | Viewed by 886
Abstract
Transforming growth factor beta (TGF-β) is ubiquitously found in bone and plays a key role in bone turnover. Mice expressing constitutively active TGF-β receptor type I (Mx1;TβRICA mice) are osteopenic. Here, we identified the candidate genes involved in bone turnover in [...] Read more.
Transforming growth factor beta (TGF-β) is ubiquitously found in bone and plays a key role in bone turnover. Mice expressing constitutively active TGF-β receptor type I (Mx1;TβRICA mice) are osteopenic. Here, we identified the candidate genes involved in bone turnover in Mx1;TβRICA mice using RNA sequencing analysis. A total of 285 genes, including 87 upregulated and 198 downregulated genes, were differentially expressed. According to the KEGG analysis, some genes were involved in osteoclast differentiation (Fcgr4, Lilrb4a), B cell receptor signaling (Cd72, Lilrb4a), and neutrophil extracellular trap formation (Hdac7, Padi4). Lilrb4 is related to osteoclast inhibition protein, whereas Hdac7 is a Runx2 corepressor that regulates osteoblast differentiation. Silencing Lilrb4 increased the number of osteoclasts and osteoclast marker genes. The knocking down of Hdac7 increased alkaline phosphatase activity, mineralization, and osteoblast marker genes. Therefore, our present study may provide an innovative idea for potential therapeutic targets and pathways in TβRI-associated bone loss. Full article
(This article belongs to the Special Issue Molecular Studies of Bone Biology and Bone Tissue)
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19 pages, 8889 KiB  
Article
Glucosamine and Silibinin Alter Cartilage Homeostasis through Glycosylation and Cellular Stresses in Human Chondrocyte Cells
by Yu-Pao Hsu, Tsung-Hsi Huang, Shu-Ting Liu, Shih-Ming Huang, Yi-Chou Chen and Chia-Chun Wu
Int. J. Mol. Sci. 2024, 25(9), 4905; https://doi.org/10.3390/ijms25094905 - 30 Apr 2024
Viewed by 1178
Abstract
Osteoarthritis is more prevalent than any other form of arthritis and is characterized by the progressive mechanical deterioration of joints. Glucosamine, an amino monosaccharide, has been used for over fifty years as a dietary supplement to alleviate osteoarthritis-related discomfort. Silibinin, extracted from milk [...] Read more.
Osteoarthritis is more prevalent than any other form of arthritis and is characterized by the progressive mechanical deterioration of joints. Glucosamine, an amino monosaccharide, has been used for over fifty years as a dietary supplement to alleviate osteoarthritis-related discomfort. Silibinin, extracted from milk thistle, modifies the degree of glycosylation of target proteins, making it an essential component in the treatment of various diseases. In this study, we aimed to investigate the functional roles of glucosamine and silibinin in cartilage homeostasis using the TC28a2 cell line. Western blots showed that glucosamine suppressed the N-glycosylation of the gp130, EGFR, and N-cadherin proteins. Furthermore, both glucosamine and silibinin differentially decreased and increased target proteins such as gp130, Snail, and KLF4 in TC28a2 cells. We observed that both compounds dose-dependently induced the proliferation of TC28a2 cells. Our MitoSOX and DCFH-DA dye data showed that 1 µM glucosamine suppressed mitochondrial reactive oxygen species (ROS) generation and induced cytosol ROS generation, whereas silibinin induced both mitochondrial and cytosol ROS generation in TC28a2 cells. Our JC-1 data showed that glucosamine increased red aggregates, resulting in an increase in the red/green fluorescence intensity ratio, while all the tested silibinin concentrations increased the green monomers, resulting in decreases in the red/green ratio. We observed increasing subG1 and S populations and decreasing G1 and G2/M populations with increasing amounts of glucosamine, while increasing amounts of silibinin led to increases in subG1, S, and G2/M populations and decreases in G1 populations in TC28a2 cells. MTT data showed that both glucosamine and silibinin induced cytotoxicity in TC28a2 cells in a dose-dependent manner. Regarding endoplasmic reticulum stress, both compounds induced the expression of CHOP and increased the level of p-eIF2α/eIF2α. With respect to O-GlcNAcylation status, glucosamine and silibinin both reduced the levels of O-GlcNAc transferase and hypoxia-inducible factor 1 alpha. Furthermore, we examined proteins and mRNAs related to these processes. In summary, our findings demonstrated that these compounds differentially modulated cellular proliferation, mitochondrial and cytosol ROS generation, the mitochondrial membrane potential, the cell cycle profile, and autophagy. Therefore, we conclude that glucosamine and silibinin not only mediate glycosylation modifications but also regulate cellular processes in human chondrocytes. Full article
(This article belongs to the Special Issue Molecular Studies of Bone Biology and Bone Tissue)
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