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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: 10 September 2024 | Viewed by 649

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

Published Papers (1 paper)

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Research

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 220
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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