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Advance in Bone Biology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 12448

Special Issue Editors

Dr. Elisa Mazzoni

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Guest Editor
Department of Chemical, Pharmaceutical and Agricultural Sciences, University of Ferrara, 44121 Ferrara, Italy
Interests: regenerative medicine; oncogenic viruses
Dr. Monica Montesi

E-Mail Website1 Website2
Guest Editor
National Research Council of Italy Institute of Science and Technology for Ceramics (ISTEC-CNR), Via Granarolo 64, I-48018 Faenza, Italy
Interests: cellular and molecular biology; material science; nanotechnology; tissue engineering and regenerative medicine; 2D and 3D cellular models; cell/biomaterial interaction
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Rosa Iaquinta

E-Mail Website
Guest Editor
Department of Medical Sciences, University of Ferrara, 64/b, Fossato di Mortara Street, 44121 Ferrara, Italy
Interests: regenerative medicine; biomaterials; stem cells; bone tissue engineering; cell biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Stem cell-based bone regeneration is currently receiving increasing research attention. Despite encouraging results on regenerative medicine, knowledge regarding bone regeneration must be evaluated. Cross-talk between immune cells and other cells in the bone regeneration process allows for bone fracture healing. Biomaterials with suitable surface modification strategies are contributing significantly to the rapid development of the field of bone tissue engineering. Moreover, biomaterial-mediated modulation of the immune response for regulating key bone regeneration events, such as osteogenesis, osteoclastogenesis, and inflammation, shows how these biomedical applications can be utilized for future bone tissue engineering applications. This Special Issue, "Advance in Bone Biology", aims to provide new information on the regulatory mechanisms of bone regeneration by focusing on the biological interaction between stem cell differentiation, the immune system, and the role of innovative materials. Authors are invited to submit original research and review articles related to these subjects.

Dr. Elisa Mazzoni
Dr. Monica Montesi
Dr. Maria Rosa Iaquinta
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

  • bone
  • stem cells
  • immunomodulation
  • biomaterial
  • regeneration
  • materials
  • biomimetic

Published Papers (7 papers)

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Research

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14 pages, 3863 KiB  
Article
M6A Demethylase Inhibits Osteogenesis of Dental Follicle Stem Cells via Regulating miR-7974/FKBP15 Pathway
by Linwei Zheng, Zhizheng Li, Bing Wang, Rui Sun, Yuqi Sun, Jiangang Ren and Jihong Zhao
Int. J. Mol. Sci. 2023, 24(22), 16121; https://doi.org/10.3390/ijms242216121 - 09 Nov 2023
Viewed by 961
Abstract
N6-methyladenosine (m6A) is the most abundant RNA modification, regulating gene expression in physiological processes. However, its effect on the osteogenic differentiation of dental follicle stem cells (DFSCs) remains unknown. Here, m6A demethylases, the fat mass and obesity-associated protein (FTO), [...] Read more.
N6-methyladenosine (m6A) is the most abundant RNA modification, regulating gene expression in physiological processes. However, its effect on the osteogenic differentiation of dental follicle stem cells (DFSCs) remains unknown. Here, m6A demethylases, the fat mass and obesity-associated protein (FTO), and alkB homolog 5 (ALKBH5) were overexpressed in DFSCs, followed by osteogenesis assay and transcriptome sequencing to explore potential mechanisms. The overexpression of FTO or ALKBH5 inhibited the osteogenesis of DFSCs, evidenced by the fact that RUNX2 independently decreased calcium deposition and by the downregulation of the osteogenic genes OCN and OPN. MiRNA profiling revealed that miR-7974 was the top differentially regulated gene, and the overexpression of m6A demethylases significantly accelerated miR-7974 degradation in DFSCs. The miR-7974 inhibitor decreased the osteogenesis of DFSCs, and its mimic attenuated the inhibitory effects of FTO overexpression. Bioinformatic prediction and RNA sequencing analysis suggested that FK506-binding protein 15 (FKBP15) was the most likely target downstream of miR-7974. The overexpression of FKBP15 significantly inhibited the osteogenesis of DFSCs via the restriction of actin cytoskeleton organization. This study provided a data resource of differentially expressed miRNA and mRNA after the overexpression of m6A demethylases in DFSCs. We unmasked the RUNX2-independent effects of m6A demethylase, miR-7974, and FKBP15 on the osteogenesis of DFSCs. Moreover, the FTO/miR-7974/FKBP15 axis and its effects on actin cytoskeleton organization were identified in DFSCs. Full article
(This article belongs to the Special Issue Advance in Bone Biology)
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20 pages, 6461 KiB  
Article
Accelerated Bone Loss in Transgenic Mice Expressing Constitutively Active TGF-β Receptor Type I
by Parichart Toejing, Nithidol Sakunrangsit, Pinyada Pho-on, Chinnatam Phetkong, Asada Leelahavanichkul, Somyoth Sridurongrit, Matthew B. Greenblatt and Sutada Lotinun
Int. J. Mol. Sci. 2023, 24(13), 10797; https://doi.org/10.3390/ijms241310797 - 28 Jun 2023
Viewed by 1279
Abstract
Transforming growth factor beta (TGF-β) is a key factor mediating the intercellular crosstalk between the hematopoietic stem cells and their microenvironment. Here, we investigated the skeletal phenotype of transgenic mice expressing constitutively active TGF-β receptor type I under the control of Mx1-Cre ( [...] Read more.
Transforming growth factor beta (TGF-β) is a key factor mediating the intercellular crosstalk between the hematopoietic stem cells and their microenvironment. Here, we investigated the skeletal phenotype of transgenic mice expressing constitutively active TGF-β receptor type I under the control of Mx1-Cre (Mx1;TβRICA mice). μCT analysis showed decreased cortical thickness, and cancellous bone volume in both femurs and mandibles. Histomorphometric analysis confirmed a decrease in cancellous bone volume due to increased osteoclast number and decreased osteoblast number. Primary osteoblasts showed decreased ALP and mineralization. Constitutive TβRI activation increased osteoclast differentiation. qPCR analysis showed that Tnfsf11/Tnfrsf11b ratio, Ctsk, Sufu, and Csf1 were increased whereas Runx2, Ptch1, and Ptch2 were decreased in Mx1;TβRICA femurs. Interestingly, Gli1, Wnt3a, Sp7, Alpl, Ptch1, Ptch2, and Shh mRNA expression were reduced whereas Tnfsf11/Tnfrsf11b ratio was increased in Mx1;TβRICA mandibles. Similarly, osteoclast-related genes were increased in Mx1;TβRICA osteoclasts whereas osteoblast-related genes were reduced in Mx1;TβRICA osteoblasts. Western blot analysis indicated that SMAD2 and SMAD3 phosphorylation was increased in Mx1;TβRICA osteoblasts, and SMAD3 phosphorylation was increased in Mx1;TβRICA osteoclasts. CTSK was increased while RUNX2 and PTCH1 was decreased in Mx1;TβRICA mice. Microindentation analysis indicated decreased hardness in Mx1;TβRICA mice. Our study indicated that Mx1;TβRICA mice were osteopenic by increasing osteoclast number and decreasing osteoblast number, possibly by suppressing Hedgehog signaling pathways. Full article
(This article belongs to the Special Issue Advance in Bone Biology)
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29 pages, 10536 KiB  
Article
MRL/MpJ Mice Resist to Age-Related and Long-Term Ovariectomy-Induced Bone Loss: Implications for Bone Regeneration and Repair
by Xueqin Gao, Xuying Sun, Haizi Cheng, Joseph J. Ruzbarsky, Michael Mullen, Matthieu Huard and Johnny Huard
Int. J. Mol. Sci. 2023, 24(3), 2396; https://doi.org/10.3390/ijms24032396 - 25 Jan 2023
Cited by 2 | Viewed by 1815
Abstract
Osteoporosis and age-related bone loss increase bone fracture risk and impair bone healing. The need for identifying new factors to prevent or treat bone loss is critical. Previously, we reported that young MRL/MpJ mice have superior bone microarchitecture and biomechanical properties as compared [...] Read more.
Osteoporosis and age-related bone loss increase bone fracture risk and impair bone healing. The need for identifying new factors to prevent or treat bone loss is critical. Previously, we reported that young MRL/MpJ mice have superior bone microarchitecture and biomechanical properties as compared to wild-type (WT) mice. In this study, MRL/MpJ mice were tested for resistance to age-related and long-term ovariectomy-induced bone loss to uncover potential beneficial factors for bone regeneration and repair. Bone tissues collected from 14-month-old MRL/MpJ and C57BL/6J (WT) mice were analyzed using micro-CT, histology, and immunohistochemistry, and serum protein markers were characterized using ELISAs or multiplex assays. Furthermore, 4-month-old MRL/MpJ and WT mice were subjected to ovariectomy (OV) or sham surgery and bone loss was monitored continuously using micro-CT at 1, 2, 4, and 6 months (M) after surgery with histology and immunohistochemistry performed at 6 M post-surgery. Sera were collected for biomarker detection using ELISA and multiplex assays at 6 M after surgery. Our results indicated that MRL/MpJ mice maintained better bone microarchitecture and higher bone mass than WT mice during aging and long-term ovariectomy. This resistance of bone loss observed in MRL/MpJ mice correlated with the maintenance of higher OSX+ osteoprogenitor cell pools, higher activation of the pSMAD5 signaling pathway, more PCNA+ cells, and a lower number of osteoclasts. Systemically, lower serum RANKL and DKK1 with higher serum IGF1 and OPG in MRL/MpJ mice relative to WT mice may also contribute to the maintenance of higher bone microarchitecture during aging and less severe bone loss after long-term ovariectomy. These findings may be used to develop therapeutic approaches to maintain bone mass and improve bone regeneration and repair due to injury, disease, and aging. Full article
(This article belongs to the Special Issue Advance in Bone Biology)
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9 pages, 3227 KiB  
Article
The Mechanism of Osteoprotegerin-Induced Osteoclast Pyroptosis In Vitro
by Jiaqiao Zhu, Yonggang Ma, Jie Wang, Yangyang Wang, Waseem Ali, Hui Zou, Hongyan Zhao, Xishuai Tong, Ruilong Song and Zongping Liu
Int. J. Mol. Sci. 2023, 24(2), 1518; https://doi.org/10.3390/ijms24021518 - 12 Jan 2023
Cited by 4 | Viewed by 1325
Abstract
Osteoprotegerin (OPG) is a new member of the tumor necrosis factor (TNF) receptor superfamily, which can inhibit the differentiation and activity of osteoclasts by binding to nuclear factor kappa B receptor activator (RANK) competitively with nuclear factor kappa B receptor activator ligand (RANKL). [...] Read more.
Osteoprotegerin (OPG) is a new member of the tumor necrosis factor (TNF) receptor superfamily, which can inhibit the differentiation and activity of osteoclasts by binding to nuclear factor kappa B receptor activator (RANK) competitively with nuclear factor kappa B receptor activator ligand (RANKL). The previous experiments found that OPG can induce apoptosis of mature osteoclasts in vitro, which can inhibit the activity of mature osteoclasts, thereby exerting its role in protecting bone tissue. In addition, pyroptosis is a new type of cell death that is different from apoptosis. It is unclear whether OPG can induce mature osteoclast pyroptosis and thereby play its role in protecting bone tissue. In this study, the results showed that compared with the control group, the survival rate of osteoclasts in the OPG group was significantly reduced, and the contents of IL-1β, IL-18, and LDH in the supernatant both increased. Many osteoclast plasma membranes were observed to rupture in bright fields, and OPG induced loss of their morphology. Flow cytometry was used to analyze the pyroptosis rate; OPG significantly increased the osteoclast pyroptosis rate. To further reveal the mechanism of OPG-induced osteoclast pyroptosis, we examined the expression level of pyroptosis-related genes and proteins, and the results found that OPG increased the expression of NLRP3, ASC, caspase-1, and GSDMD-N compared with the control group. In summary, OPG can induce osteoclast pyroptosis, and its mechanism is related to the expression levels of ASC, NLRP3, caspase 1 and GSDMD, which were included in the classical pathway of pyroptosis. Full article
(This article belongs to the Special Issue Advance in Bone Biology)
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14 pages, 3513 KiB  
Article
ERK Inhibition Increases RANKL-Induced Osteoclast Differentiation in RAW 264.7 Cells by Stimulating AMPK Activation and RANK Expression and Inhibiting Anti-Osteoclastogenic Factor Expression
by Eun-Bi Choi, Taiwo Samuel Agidigbi, In-Soon Kang and Chaekyun Kim
Int. J. Mol. Sci. 2022, 23(21), 13512; https://doi.org/10.3390/ijms232113512 - 04 Nov 2022
Cited by 8 | Viewed by 1758
Abstract
Bone absorption is necessary for the maintenance of bone homeostasis. An osteoclast (OC) is a monocyte–macrophage lineage cell that absorbs bone tissue. Extracellular signal-regulated kinases (ERKs) are known to play important roles in regulating OC growth and differentiation. In this study, we examined [...] Read more.
Bone absorption is necessary for the maintenance of bone homeostasis. An osteoclast (OC) is a monocyte–macrophage lineage cell that absorbs bone tissue. Extracellular signal-regulated kinases (ERKs) are known to play important roles in regulating OC growth and differentiation. In this study, we examined specific downstream signal pathways affected by ERK inhibition during OC differentiation. Our results showed that the ERK inhibitors PD98059 and U0126 increased receptor activator of NF-κB ligand (RANKL)-induced OC differentiation in RAW 264.7 cells, implying a negative role in OC differentiation. This is supported by the effect of ERK2-specific small interfering RNA on increasing OC differentiation. In contrast to our findings regarding the RAW 264.7 cells, the ERK inhibitors attenuated the differentiation of bone marrow-derived cells into OCs. The ERK inhibitors significantly increased the phosphorylation of adenosine 5′-monophosphate-activated protein kinase (AMPK) but not the activation of p38 MAPK, Lyn, and mTOR. In addition, while the ERK inhibition increased the expression of the RANKL receptor RANK, it decreased the expression of negative mediators of OC differentiation, such as interferon regulatory factor-8, B-cell lymphoma 6, and interferon-γ. These dichotomous effects of ERK inhibition suggest that while ERKs may play positive roles in bone marrow-derived cells, ERKs may also play negative regulatory roles in RAW 264.7 cells. These data provide important information for drug development utilizing ERK inhibitors in OC-related disease treatment. Full article
(This article belongs to the Special Issue Advance in Bone Biology)
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10 pages, 969 KiB  
Communication
Reciprocal Alterations in Osteoprogenitor and Immune Cell Populations in Rheumatoid Synovia
by Katarina Barbarić Starčević, Nina Lukač, Mislav Jelić, Alan Šućur, Danka Grčević and Nataša Kovačić
Int. J. Mol. Sci. 2022, 23(20), 12379; https://doi.org/10.3390/ijms232012379 - 16 Oct 2022
Viewed by 1057
Abstract
Rheumatoid arthritis (RA) is chronic, autoimmune joint inflammation characterized by irreversible joint destruction. Besides increased resorption, destruction is a result of decreased bone formation, due to suppressed differentiation and function of the mesenchymal lineage-derived osteoblasts in inflammatory milieu. In this study, we analyzed [...] Read more.
Rheumatoid arthritis (RA) is chronic, autoimmune joint inflammation characterized by irreversible joint destruction. Besides increased resorption, destruction is a result of decreased bone formation, due to suppressed differentiation and function of the mesenchymal lineage-derived osteoblasts in inflammatory milieu. In this study, we analyzed the cellular composition of synovial tissue from 11 RA and 10 control patients harvested during planned surgeries in order to characterize resident synovial progenitor populations. Synovial cells were released by collagenase, and labeled for flow cytometry by two antibody panels: 1. CD3-FITC, CD14-PE, 7-AAD, CD11b-PECy7, CD235a-APC, CD19-APCeF780; and 2. 7-AAD, CD105-PECy7, CD45/CD31/CD235a-APC, and CD200-APCeF780. The proportions of lymphocytes (CD3+, CD19+) and myeloid (CD11b+, CD14+) cells were higher in synovial tissue from the patients with RA than in the controls. Among non-hematopoietic (CD45−CD31−CD235a−) cells, there was a decrease in the proportion of CD200+CD105− and increase in the proportion of CD200−CD105+ cells in synovial tissue from the patients with RA in comparison to the control patients. The proportions of both populations were associated with inflammatory activity and could discriminate between the RA and the controls. Full article
(This article belongs to the Special Issue Advance in Bone Biology)
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Review

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27 pages, 2687 KiB  
Review
Hypoxia-Inducible Factors Signaling in Osteogenesis and Skeletal Repair
by Qiuyue Qin, Yiping Liu, Zhen Yang, Maierhaba Aimaijiang, Rui Ma, Yixin Yang, Yidi Zhang and Yanmin Zhou
Int. J. Mol. Sci. 2022, 23(19), 11201; https://doi.org/10.3390/ijms231911201 - 23 Sep 2022
Cited by 15 | Viewed by 3039
Abstract
Sufficient oxygen is required to maintain normal cellular and physiological function, such as a creature’s development, breeding, and homeostasis. Lately, some researchers have reported that both pathological hypoxia and environmental hypoxia might affect bone health. Adaptation to hypoxia is a pivotal cellular event [...] Read more.
Sufficient oxygen is required to maintain normal cellular and physiological function, such as a creature’s development, breeding, and homeostasis. Lately, some researchers have reported that both pathological hypoxia and environmental hypoxia might affect bone health. Adaptation to hypoxia is a pivotal cellular event in normal cell development and differentiation and in pathological settings such as ischemia. As central mediators of homeostasis, hypoxia-inducible transcription factors (HIFs) can allow cells to survive in a low-oxygen environment and are essential for the regulation of osteogenesis and skeletal repair. From this perspective, we summarized the role of HIF-1 and HIF-2 in signaling pathways implicated in bone development and skeletal repair and outlined the molecular mechanism of regulation of downstream growth factors and protein molecules such as VEGF, EPO, and so on. All of these present an opportunity for developing therapies for bone regeneration. Full article
(This article belongs to the Special Issue Advance in Bone Biology)
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