Osteoblasts subjected to tensile force induce osteoclastic differentiation of murine macrophages in a coculture system

Chen, Yi-Jyun; Shie, Ming‐You; Hung, Chi-Jr; Liu, Shiau-Lee; Huang, Tsui‐Hsien; Kao, Chia‐Tze

doi:10.1016/j.jds.2013.11.003

Cited by 7 publications

(4 citation statements)

References 29 publications

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“…A previous study has shown that VEGF release (MMP-dependent) results in the formation of a more regular vasculature compared with passive VEGF release via diffusion [12]. Several studies on multi-type cell co-culture have been proved to achieve promoted cellular differentiation-related expression that deeply relies on the interactive biological stimulation between cells [34]. For example, during the bone regeneration process, osteoblast differentiation can be stimulated by introducing a blood vessel-forming cell system that in the meantime can be stimulated by the surrounding osteoblast − ECM environment to develop into blood vessels [35].…”

Section: Discussionmentioning

confidence: 99%

The synergistic effect on osteogenic differentiation of human mesenchymal stem cells by diode laser-treated stimulating human umbilical vein endothelial cells

et al. 2015

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Angiogenesis plays an important role in determining the biostimulation of bone regeneration, in either new bone or blood vessel formation. Human umbilical cord cells (HUVECs) are important effector cells in angiogenesis and are indispensable for osteogenesis and for their heterogeneity and plasticity. However, there are very few studies about the effects of HUVECs on diode laser-stimulated/regulated osteogenesis. In this study, we used diode laser as a model biostimulation to examine the role of HUVECs on laser-stimulated osteogenesis. Several bone formation-related proteins were also significantly up-regulated by the diode laser stimulation, indicating that HUVECs may participate in diode laser-stimulated osteogenesis. Interestingly, when human mesenchymal stem cells (hMSCs) cultured with HUVECs were diode laser-treated, the osteogenesis differentiation of the hMSCs was significantly promoted, indicating the important role of HUVECs in diode laser-enhanced osteogenesis. Adequately activated HUVECs are vital for the success of diode laser-stimulated hard-tissue regeneration. These findings provided valuable insights into the mechanism of diode laser-stimulated osteogenic differentiation, and a strategy to optimize the evaluation system for the in vitro osteogenesis capacity of laser treatment in periodontal repair.

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Section: Discussionmentioning

confidence: 99%

The synergistic effect on osteogenic differentiation of human mesenchymal stem cells by diode laser-treated stimulating human umbilical vein endothelial cells

et al. 2015

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“…The classically activated inflammatory macrophages cells affected osteogenic differentiation in hMSCs [28]. Bone reconstitution research must consider molecular interactions and several pathways [29]. Inhibiting osteoblast secreted RANKL or antagonizing RANKL actions on osteoclasts might be a defended mechanism for preventing excessive osteoclast differentiation [30].…”

Section: Discussionmentioning

confidence: 99%

Antiosteoclastogenesis activity of a CO₂laser antagonizing receptor activator for nuclear factor kappaB ligand-induced osteoclast differentiation of murine macrophages

Kuo¹,

Kao²,

Fang³

et al. 2015

Laser Phys. Lett.

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Macrophage cells are the important effector cells in the immune reaction which are indispensable for osteoclastogenesis; their heterogeneity and plasticity renders macrophages a primer target for immune system modulation. In recent years, there have been very few studies about the effects of macrophage cells on laser treatment-regulated osteoclastogenesis. In this study, RAW 264.7 macrophage cells were treated with RANKL to regulate osteoclastogenesis. We used a CO 2 laser as a model biostimulation to investigate the role of osteoclastogenic. We also evaluated cell viability, cell death and cathepsin K expression. The CO 2 laser inhibited a receptor activator of the NF-ĸB ligand (RANKL)-induced formation of osteoclasts during the osteoclast differentiation process. It was also found that irradiation for two times reduced RANKL-enhanced TRAP activity in a dose-dependent manner. Furthermore, CO 2 lasertreatment diminished the expression and secretion of cathepsin K elevated by RANKL and was concurrent with the inhibition of TRAF6 induction and NF-ĸB activation. The current report demonstrates that CO 2 laser abrogated RANKL-induced osteoclastogenesis by retarding osteoclast differentiation. The CO 2 laser can modulate every cell through dose-dependent in vitro RANKL-mediated osteoclastogenesis, such as the proliferation and fusion of preosteoclasts and the maturation of osteoclasts. Therefore, the current results serve as an improved explanation of the cellular roles of macrophage cell populations in osteoclastogenesis as well as in alveolar bone remodeling by CO 2 laser-treatment.

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“…Shown to be present in calcified plaques, osteoclast-like cells are thought to be the missing link between the RANKL/OPG pathway and canonical WNT [66,67]. Shown to interact through osteoblast-induced macrophage differentiation to osteoclasts in vitro, the balance between these two reciprocal pathways is predicted to be disrupted by mechanical overstimulation [68]. As RANKL is deactivated from WNT-expressed OPG, deposited hydroxyapatite overwhelms the immune system's ability to remove it.…”

Section: Wnt Bone Remodeling and Mechanical Strainmentioning

confidence: 99%

Mechanisms of the Osteogenic Switch of Smooth Muscle Cells in Vascular Calcification: WNT Signaling, BMPs, Mechanotransduction, and EndMT

et al. 2020

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Characterized by the hardening of arteries, vascular calcification is the deposition of hydroxyapatite crystals in the arterial tissue. Calcification is now understood to be a cell-regulated process involving the phenotypic transition of vascular smooth muscle cells into osteoblast-like cells. There are various pathways of initiation and mechanisms behind vascular calcification, but this literature review highlights the wingless-related integration site (WNT) pathway, along with bone morphogenic proteins (BMPs) and mechanical strain. The process mirrors that of bone formation and remodeling, as an increase in mechanical stress causes osteogenesis. Observing the similarities between the two may aid in the development of a deeper understanding of calcification. Both are thought to be regulated by the WNT signaling cascade and bone morphogenetic protein signaling and can also be activated in response to stress. In a pro-calcific environment, integrins and cadherins of vascular smooth muscle cells respond to a mechanical stimulus, activating cellular signaling pathways, ultimately resulting in gene regulation that promotes calcification of the vascular extracellular matrix (ECM). The endothelium is also thought to contribute to vascular calcification via endothelial to mesenchymal transition, creating greater cell plasticity. Each of these factors contributes to calcification, leading to increased cardiovascular mortality in patients, especially those suffering from other conditions, such as diabetes and kidney failure. Developing a better understanding of the mechanisms behind calcification may lead to the development of a potential treatment in the future.

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Osteoblasts subjected to tensile force induce osteoclastic differentiation of murine macrophages in a coculture system

Cited by 7 publications

References 29 publications

The synergistic effect on osteogenic differentiation of human mesenchymal stem cells by diode laser-treated stimulating human umbilical vein endothelial cells

The synergistic effect on osteogenic differentiation of human mesenchymal stem cells by diode laser-treated stimulating human umbilical vein endothelial cells

Antiosteoclastogenesis activity of a CO₂laser antagonizing receptor activator for nuclear factor kappaB ligand-induced osteoclast differentiation of murine macrophages

Mechanisms of the Osteogenic Switch of Smooth Muscle Cells in Vascular Calcification: WNT Signaling, BMPs, Mechanotransduction, and EndMT

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Osteoblasts subjected to tensile force induce osteoclastic differentiation of murine macrophages in a coculture system

Cited by 7 publications

References 29 publications

The synergistic effect on osteogenic differentiation of human mesenchymal stem cells by diode laser-treated stimulating human umbilical vein endothelial cells

The synergistic effect on osteogenic differentiation of human mesenchymal stem cells by diode laser-treated stimulating human umbilical vein endothelial cells

Antiosteoclastogenesis activity of a CO2laser antagonizing receptor activator for nuclear factor kappaB ligand-induced osteoclast differentiation of murine macrophages

Mechanisms of the Osteogenic Switch of Smooth Muscle Cells in Vascular Calcification: WNT Signaling, BMPs, Mechanotransduction, and EndMT

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Antiosteoclastogenesis activity of a CO₂laser antagonizing receptor activator for nuclear factor kappaB ligand-induced osteoclast differentiation of murine macrophages