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Osteoclastogenesis and Osteogenesis 2.0

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

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 29271

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Prof. Dr. Jung Eun Kim

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Department of Molecular Medicine, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea
Interests: osteoblast/osteoclast differentiation; bone remodeling; bone development and homeostasis; bone metastasis; musculoskeletal diseases
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Special Issue Information

Dear Colleagues,

Welcome to the Special Issue, entitled “Osteoclastogenesis and Osteogenesis”, of the Biochemistry Section of the International Journal of Molecular Sciences.

Bone is a highly dynamic tissue that is continuously remodeled to attain and maintain optimal bone integrity, mass, and strength. Normal bone remodeling is tightly regulated by a balance between osteoclastic bone resorption and osteoblastic bone formation. However, the physiological condition can be changed by various factors, which can lead to an imbalance of bone remodeling and the development of bone diseases such as osteoporosis. Thus, osteoclastogenesis and osteogenesis are the most basic, but most essential, mechanisms in bone biology. This Special Issue focuses on novel molecular mechanisms of osteoblasts and osteoclasts contributing to bone remodeling and provides a powerful platform for elucidating novel insights into bone pathophysiology. We very much welcome the submission of original research articles and comprehensive reviews.

Prof. Dr. Jung Eun Kim
Guest Editor

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Keywords

osteoblast
osteocyte
osteoclast
mesenchymal stem cell
bone lining cell
hematopoietic stem cell
cell differentiation
bone remodeling
bone pathophysiology

Published Papers (11 papers)

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Research

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17 pages, 2509 KiB

Open AccessArticle

Ectodysplasin A1 Deficiency Leads to Osteopetrosis-like Changes in Bones of the Skull Associated with Diminished Osteoclastic Activity

by Christine Schweikl, Sigrun Maier-Wohlfart, Holm Schneider and Jung Park

Int. J. Mol. Sci. 2022, 23(20), 12189; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012189 - 13 Oct 2022

Cited by 2 | Viewed by 1534

Abstract

Pathogenic variants of the gene Eda cause X-linked hypohidrotic ectodermal dysplasia (XLHED), which is characterized by structural abnormalities or lack of ectodermal appendages. Signs of dysplasia are not restricted to derivatives of the ectodermal layer, but mesodermal abnormalities, such as craniofacial dysmorphism, are also frequently observed, suggesting close reciprocal interactions between the ectoderm and mesoderm; however, a causal link has remained unsubstantiated. We investigated the functional impact of defective ectodysplasin A1 (Eda1) signaling on postnatal bone homeostasis in Eda1-deficient Tabby mice. Interestingly, Eda1 was detected in wild-type mouse calvariae throughout postnatal lifetime. In calvariae, bone-lining Osterix (Osx)+ osteoblasts stained positive for Eda1, and osteoclasts were revealed as Eda receptor (Edar)-positive. Moreover, adult Eda1-deficient calvarial bone showed osteopetrosis-like changes with significantly diminished marrow space, which was maintained during adulthood. Concomitantly with osteopetrosis-like changes, Tabby calvarial bone and Tabby bone marrow-derived osteoclasts had far less osteoclastic activity-associated co-enzymes including cathepsin K, Mmp9, Trap, and Tcirg1 (V-type proton ATPase a3 subunit) compared with wild-type calvariae in vivo or osteoclasts in vitro, indicating that Eda1 deficiency may affect the activity of osteoclasts. Finally, we confirmed that nuclear Nfatc1-positive osteoclasts were strongly diminished during mature osteoclastic differentiation under M-CSF and RANKL in the Tabby model, while Fc-EDA treatment of Tabby-derived osteoclasts significantly increased nuclear translocation of Nfatc1. Furthermore, we identified enhanced Nfatc1 and NF-κB transcriptional activity following Fc-EDA treatment in vitro using luciferase assays. Overall, the results indicate that diminished expressions of osteoclastic activity-associated co-enzymes may lead to disturbed bone homeostasis in Tabby calvariae postnatally. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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18 pages, 3833 KiB

Open AccessArticle

Psychostimulants Modafinil, Atomoxetine and Guanfacine Impair Bone Cell Differentiation and MSC Migration

by Nele Wagener, Wolfgang Lehmann, Lukas Weiser, Katharina Jäckle, Pietro Di Fazio, Arndt F. Schilling and Kai O. Böker

Int. J. Mol. Sci. 2022, 23(18), 10257; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231810257 - 06 Sep 2022

Cited by 1 | Viewed by 2890

Abstract

Attention deficit hyperactivity disorder (ADHD) is one of the most common worldwide mental disorders in children, young and adults. If left untreated, the disorder can continue into adulthood. The abuse of ADHD-related drugs to improve mental performance for studying, working and everyday life is also rising. The potentially high number of subjects with controlled or uncontrolled use of such substances increases the impact of possible side effects. It has been shown before that the early ADHD drug methylphenidate influences bone metabolism negatively. This study focused on the influence of three more recent cognitive enhancers, modafinil, atomoxetine and guanfacine, on the differentiation of mesenchymal stem cells to osteoblasts and on their cell functions, including migration. Human mesenchymal stem cells (hMSCs) were incubated with a therapeutic plasma dosage of modafinil, atomoxetine and guanfacine. Gene expression analyses revealed a high beta-2 adrenoreceptor expression in hMSC, suggesting it as a possible pathway to stimulate action. In bone formation assays, all three cognitive enhancers caused a significant decrease in the mineralized matrix and an early slight reduction of cell viability without triggering apoptosis or necrosis. While there was no effect of the three substances on early differentiation, they showed differing effects on the expression of osterix (OSX), receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) in the later stages of osteoblast development, suggesting alternative modes of action. All three substances significantly inhibited hMSC migration. This effect could be rescued by a selective beta-blocker (Imperial Chemical Industries ICI-118,551) in modafinil and atomoxetine, suggesting mediation via beta-2 receptor stimulation. In conclusion, modafinil, atomoxetine and guanfacine negatively influence hMSC differentiation to bone-forming osteoblasts and cell migration through different intracellular pathways. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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12 pages, 2578 KiB

Open AccessArticle

Cyclophilin A Promotes Osteoblast Differentiation by Regulating Runx2

by Meiyu Piao, Sung Ho Lee, Myeong Ji Kim, Joong-Kook Choi, Chang-Yeol Yeo and Kwang Youl Lee

Int. J. Mol. Sci. 2022, 23(16), 9244; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23169244 - 17 Aug 2022

Cited by 2 | Viewed by 1521

Abstract

Cyclophilin A (CypA) is a ubiquitously expressed and highly conserved protein with peptidyl-prolyl cis-trans isomerase activity that is involved in various biological activities by regulating protein folding and trafficking. Although CypA has been reported to positively regulate osteoblast differentiation, the mechanistic details remain largely unknown. In this study, we aimed to elucidate the mechanism of CypA-mediated regulation of osteoblast differentiation. Overexpression of CypA promoted osteoblast differentiation in bone morphogenic protein 4 (BMP4)-treated C2C12 cells, while knockdown of CypA inhibited osteoblast differentiation in BMP4-treated C2C12. CypA and Runx2 were shown to interact based on immunoprecipitation experiments and CypA increased Runx2 transcriptional activity in a dose-dependent manner. Our results indicate that this may be because CypA can increase the DNA binding affinity of Runx2 to Runx2 binding sites such as osteoblast-specific cis-acting element 2. Furthermore, to identify factors upstream of CypA in the regulation of osteoblast differentiation, various kinase inhibitors known to affect osteoblast differentiation were applied during osteogenesis. Akt inhibition resulted in the most significant suppression of osteogenesis in BMP4-induced C2C12 cells overexpressing CypA. Taken together, our results show that CypA positively regulates osteoblast differentiation by increasing the DNA binding affinity of Runx2, and Akt signaling is upstream of CypA. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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20 pages, 4467 KiB

Open AccessArticle

Changes in Metabolism and Mitochondrial Bioenergetics during Polyethylene-Induced Osteoclastogenesis

by Nur Shukriyah Mohamad Hazir, Nor Hamdan Mohamad Yahaya, Muhamad Syahrul Fitri Zawawi, Hanafi Ahmad Damanhuri, Norazlina Mohamed and Ekram Alias

Int. J. Mol. Sci. 2022, 23(15), 8331; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158331 - 28 Jul 2022

Cited by 2 | Viewed by 1754

Abstract

Changes in mitochondrial bioenergetics are believed to take place during osteoclastogenesis. This study aims to assess changes in mitochondrial bioenergetics and reactive oxygen species (ROS) levels during polyethylene (PE)-induced osteoclastogenesis in vitro. For this purpose, RAW264.7 cells were cultured for nine days and allowed to differentiate into osteoclasts in the presence of PE and RANKL. The total TRAP-positive cells, resorption activity, expression of osteoclast marker genes, ROS level, mitochondrial bioenergetics, glycolysis, and substrate utilization were measured. The effect of tocotrienols-rich fraction (TRF) treatment (50 ng/mL) on those parameters during PE-induced osteoclastogenesis was also studied. During PE-induced osteoclastogenesis, as depicted by an increase in TRAP-positive cells and gene expression of osteoclast-related markers, higher proton leak, higher extracellular acidification rate (ECAR), as well as higher levels of ROS and NADPH oxidases (NOXs) were observed in the differentiated cells. The oxidation level of some substrates in the differentiated group was higher than in other groups. TRF treatment significantly reduced the number of TRAP-positive osteoclasts, bone resorption activity, and ROS levels, as well as modulating the gene expression of antioxidant-related genes and mitochondrial function. In conclusion, changes in mitochondrial bioenergetics and substrate utilization were observed during PE-induced osteoclastogenesis, while TRF treatment modulated these changes. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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15 pages, 3595 KiB

Open AccessArticle

NLRP3 Inflammasome Negatively Regulates RANKL-Induced Osteoclastogenesis of Mouse Bone Marrow Macrophages but Positively Regulates It in the Presence of Lipopolysaccharides

by Mohammad Ibtehaz Alam, Megumi Mae, Fatima Farhana, Masayuki Oohira, Yasunori Yamashita, Yukio Ozaki, Eiko Sakai and Atsutoshi Yoshimura

Int. J. Mol. Sci. 2022, 23(11), 6096; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23116096 - 29 May 2022

Cited by 10 | Viewed by 2623

Abstract

In inflammatory bone diseases such as periodontitis, the nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing 3 (NLRP3) inflammasome accelerates bone resorption by promoting proinflammatory cytokine IL-1β production. However, the role of the NLRP3 inflammasome in physiological bone remodeling remains unclear. Here, we investigated its role in osteoclastogenesis in the presence and absence of lipopolysaccharide (LPS), a Gram-negative bacterial component. When bone marrow macrophages (BMMs) were treated with receptor activator of nuclear factor-κB ligand (RANKL) in the presence of NLRP3 inflammasome inhibitors, osteoclast formation was promoted in the absence of LPS but attenuated in its presence. BMMs treated with RANKL and LPS produced IL-1β, and IL-1 receptor antagonist inhibited osteoclastogenesis, indicating IL-1β involvement. BMMs treated with RANKL alone produced no IL-1β but increased reactive oxygen species (ROS) production. A ROS inhibitor suppressed apoptosis-associated speck-like protein containing a caspase-1 recruitment domain (ASC) speck formation and NLRP3 inflammasome inhibitors abrogated cytotoxicity in BMMs treated with RANKL, indicating that RANKL induces pyroptotic cell death in BMMs by activating the NLRP3 inflammasome via ROS. This suggests that the NLRP3 inflammasome promotes osteoclastogenesis via IL-1β production under infectious conditions, but suppresses osteoclastogenesis by inducing pyroptosis in osteoclast precursors under physiological conditions. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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12 pages, 3858 KiB

Open AccessArticle

7-Ketocholesterol-Induced Micro-RNA-107-5p Increases Number and Activity of Osteoclasts by Targeting MKP1

by Guoen Li, Ok-Joo Sul, Rina Yu and Hye-Seon Choi

Int. J. Mol. Sci. 2022, 23(7), 3697; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073697 - 28 Mar 2022

Cited by 5 | Viewed by 1752

Abstract

Osteoclasts (OCs), which are responsible for bone resorption, play a critical role in cholesterol-induced bone loss and recent studies have suggested that various micro-RNAs (miRs) contribute to modulating OCs. We hypothesized that 7-ketocholesterol (7-KC), a metabolite responsible for cholesterol-induced bone loss, induces miR-107-5p, which affects OCs. Overexpression and knock-down of miR-107-5p were performed using miR-107-5p mimic and anti-miR-107-5p, respectively. The effects of miR-107-5p on OCs were analyzed by tartrate-resistant alkaline phosphatase staining, qPCR, and Western blot. MiR-107-5p was upregulated after 7-KC exposure in receptor activator of nuclear factor kappa-Β ligand-stimulated OCs. Furthermore, miR-107-5p upregulation was also observed in tibiae from an atherogenic diet-fed mice compared with mice fed with a normal diet. MiR-107-5p overexpression enhanced the area and number of OCs, whereas inhibiting the endogenous expression of miR-107-5p generated by 7-KC had the opposite effect. Among the possible candidates, mitogen-activated protein kinase phosphatase-1, a stress-responsive dual-specificity phosphatase that inactivates mitogen-activated protein kinase (MKP1), has been proven to be a target gene of miR-107-5p, as demonstrated by the direct interaction between miR-107-5p and the 3′-untranslated region of MKP1. Collectively, our findings demonstrate that 7-KC-induced miR-107-5p promotes differentiation and function of OCs by downregulating MKP1. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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14 pages, 1542 KiB

Open AccessArticle

The ATF3–OPG Axis Contributes to Bone Formation by Regulating the Differentiation of Osteoclasts, Osteoblasts, and Adipocytes

by Jung Ha Kim, Kabsun Kim, Inyoung Kim, Semun Seong, Jeong-Tae Koh and Nacksung Kim

Int. J. Mol. Sci. 2022, 23(7), 3500; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23073500 - 23 Mar 2022

Cited by 3 | Viewed by 2110

Abstract

Activating transcription factor 3 (ATF3) has been identified as a negative regulator of osteoblast differentiation in in vitro study. However, it was not associated with osteoblast differentiation in in vivo study. To provide an understanding of the discrepancy between the in vivo and in vitro findings regarding the function of ATF3 in osteoblasts, we investigated the unidentified roles of ATF3 in osteoblast biology. ATF3 enhanced osteoprotegerin (OPG) production, not only in osteoblast precursor cells, but also during osteoblast differentiation and osteoblastic adipocyte differentiation. In addition, ATF3 increased nodule formation in immature osteoblasts and decreased osteoblast-dependent osteoclast formation, as well as the transdifferentiation of osteoblasts to adipocytes. However, all these effects were reversed by the OPG neutralizing antibody. Taken together, these results suggest that ATF3 contributes to bone homeostasis by regulating the differentiation of various cell types in the bone microenvironment, including osteoblasts, osteoclasts, and adipocytes via inducing OPG production. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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17 pages, 3130 KiB

Open AccessArticle

Micro-Osteoperforations Induce TNF-α Expression and Accelerate Orthodontic Tooth Movement via TNF-α-Responsive Stromal Cells

by Ria Kinjo, Hideki Kitaura, Saika Ogawa, Fumitoshi Ohori, Takahiro Noguchi, Aseel Marahleh, Yasuhiko Nara, Adya Pramusita, Jinghan Ma, Kayoko Kanou and Itaru Mizoguchi

Int. J. Mol. Sci. 2022, 23(6), 2968; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23062968 - 09 Mar 2022

Cited by 2 | Viewed by 3736

Abstract

Micro-osteoperforations (MOPs) have been reported to accelerate orthodontic tooth movement (OTM), and tumor necrosis factor (TNF)-α has been reported to play a crucial role in OTM. In this report, the influence of MOPs during OTM was analyzed. We evaluated the expression of TNF-α with and without MOPs by RT-PCR analysis. A Ni-Ti closed coil spring was fixed between the maxillary left first molar and the incisors as an OTM mouse model to move the first molar in the mesial direction. MOPs were prepared on the lingual side and mesial side of the upper first molars. Furthermore, to investigate the target cell of TNF-α for osteoclast formation during OTM with MOPs in vivo, we created four types of chimeric mice in which bone marrow of wild-type (WT) or TNF receptor 1- and 2-deficient mice (KO) was transplanted into lethally irradiated WT or KO mice. The results showed that MOPs increased TNF-α expression, the distance of tooth movement and osteoclast formation significantly. Furthermore, mice with TNF-α-responsive stromal cells showed a significant increase in tooth movement and number of osteoclasts by MOPs. We conclude that MOPs increase TNF-α expression, and tooth movement is dependent on TNF-α-responsive stromal cells. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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19 pages, 9693 KiB

Open AccessArticle

Serial Passaging of RAW 264.7 Cells Modulates Intracellular AGE Formation and Downregulates RANKL-Induced In Vitro Osteoclastogenesis

by Tanzima Tarannum Lucy, A. N. M. Mamun-Or-Rashid, Masayuki Yagi and Yoshikazu Yonei

Int. J. Mol. Sci. 2022, 23(4), 2371; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23042371 - 21 Feb 2022

Cited by 3 | Viewed by 2942

Abstract

The passage number of cells refers to the number of subculturing processes that the cells have undergone. The effect of passage number on morphological and phenotypical characteristics of cells is of great importance. Advanced glycation end products have also been associated with cell functionality and characteristics. Murine monocyte RAW 264.7 cells differentiate into osteoclasts upon receptor activation caused by nuclear factor-kappa-Β ligand (RANKL) treatment. This study aims to identify the role of passage number on intracellular advanced glycation end products (AGEs) formation and osteoclastogenic differentiation of RAW 264.7 cells. Western blotting was performed to check intracellular AGE formation along with fluorometric analysis using a microplate reader. Tartrate-resistant acid phosphatase (TRAP) staining was performed to check osteoclastogenic differentiation, and qPCR was realized to check the responsible mRNA expression. Immunofluorescence was used to check the morphological changes. Intracellular AGE formation was increased with passaging, and the higher passage number inhibited multinucleated osteoclastogenic differentiation. Osteoclastogenic gene expression also showed a reducing trend in higher passages, along with a significant reduction in F-actin ring size and number. Lower passages should be used to avoid the effects of cell subculturing in in vitro osteoclastogenesis study using RAW 264.7 cells. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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Review

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19 pages, 1135 KiB

Open AccessReview

A Review of Signaling Transduction Mechanisms in Osteoclastogenesis Regulation by Autophagy, Inflammation, and Immunity

by Xishuai Tong, Gengsheng Yu, Xiaohui Fu, Ruilong Song, Jianhong Gu and Zongping Liu

Int. J. Mol. Sci. 2022, 23(17), 9846; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23179846 - 30 Aug 2022

Cited by 7 | Viewed by 2438

Abstract

Osteoclastogenesis is an ongoing rigorous course that includes osteoclast precursors fusion and bone resorption executed by degradative enzymes. Osteoclastogenesis is controlled by endogenous signaling and/or regulators or affected by exogenous conditions and can also be controlled both internally and externally. More evidence indicates that autophagy, inflammation, and immunity are closely related to osteoclastogenesis and involve multiple intracellular organelles (e.g., lysosomes and autophagosomes) and certain inflammatory or immunological factors. Based on the literature on osteoclastogenesis induced by different regulatory aspects, emerging basic cross-studies have reported the emerging disquisitive orientation for osteoclast differentiation and function. In this review, we summarize the partial potential therapeutic targets for osteoclast differentiation and function, including the signaling pathways and various cellular processes. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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16 pages, 1752 KiB

Open AccessReview

Toxic Effects of Indoxyl Sulfate on Osteoclastogenesis and Osteoblastogenesis

by Jia-Fwu Shyu, Wen-Chih Liu, Cai-Mei Zheng, Te-Chao Fang, Yi-Chou Hou, Chiz-Tzung Chang, Ting-Ying Liao, Yin-Cheng Chen and Kuo-Cheng Lu

Int. J. Mol. Sci. 2021, 22(20), 11265; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222011265 - 19 Oct 2021

Cited by 10 | Viewed by 4393

Abstract

Uremic toxins, such as indoxyl sulfate (IS) and kynurenine, accumulate in the blood in the event of kidney failure and contribute to further bone damage. To maintain the homeostasis of the skeletal system, bone remodeling is a persistent process of bone formation and bone resorption that depends on a dynamic balance of osteoblasts and osteoclasts. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that regulates the toxic effects of uremic toxins. IS is an endogenous AhR ligand and is metabolized from tryptophan. In osteoclastogenesis, IS affects the expression of the osteoclast precursor nuclear factor of activated T cells, cytoplasmic 1 (NFATc1) through AhR signaling. It is possible to increase osteoclast differentiation with short-term and low-dose IS exposure and to decrease differentiation with long-term and/or high-dose IS exposure. Coincidentally, during osteoblastogenesis, through the AhR signaling pathway, IS inhibits the phosphorylation of ERK, and p38 reduces the expression of the transcription factor 2 (Runx2), disturbing osteoblastogenesis. The AhR antagonist resveratrol has a protective effect on the IS/AhR pathway. Therefore, it is necessary to understand the multifaceted role of AhR in CKD, as knowledge of these transcription signals could provide a safe and effective method to prevent and treat CKD mineral bone disease. Full article

(This article belongs to the Special Issue Osteoclastogenesis and Osteogenesis 2.0)

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