Pulsed electromagnetic field inhibits RANKL-dependent osteoclastic differentiation in RAW264.7 cells through the Ca 2+ -calcineurin-NFATc1 signaling pathway

Zhang, Jie; Xu, Haixia; Han, Zhen; Chen, Ping; Yu, Qiang; Lei, Yutian; Li, Zongze; Zhao, Ming; Tian, Jinhui

doi:10.1016/j.bbrc.2016.11.056

Cited by 26 publications

(26 citation statements)

References 34 publications

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“…Moreover, our results also demonstrate that osteoclastogenesis‐associated gene expression was also suppressed by 0.5 mT PEMF, but enhanced by 3 mT PEMF. Considering the confirmed effects of PEMF on regulating osteoclastogenesis [Chang et al, ; Chang et al, ; Zhang et al, ], no positive control (chemicals or physical factors which are already known to regulate osteoclast activity and function) was used in our present study, which may be a limitation of our study. Our present findings reveal an important intensity window for low‐intensity PEMF in regulating bone resorption with diverse nature for modulating osteoclastogenesis and apoptosis, and can enrich our basic knowledge for understanding the mechanism of PEMF‐mediated inhibition of osteoclast activities.…”

Section: Discussionmentioning

confidence: 99%

Differential intensity‐dependent effects of pulsed electromagnetic fields on RANKL‐induced osteoclast formation, apoptosis, and bone resorbing ability in RAW264.7 cells

Wang

Liu

Yang

et al. 2017

Bioelectromagnetics

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Pulsed electromagnetic fields (PEMF) have been proven to be effective for promoting bone mass and regulating bone turnover both experimentally and clinically. However, the exact mechanisms for the regulation of PEMF on osteoclastogenesis as well as optical exposure parameters of PEMF on inhibiting osteoclastic activities and functions remain unclear, representing significant limitations for extensive scientific application of PEMF in clinics. In this study, RAW264.7 cells incubated with RANKL were exposed to 15 Hz PEMF (2 h/day) at various intensities (0.5, 1, 2, and 3 mT) for 7 days. We demonstrate that bone resorbing capacity was significantly decreased by 0.5 mT PEMF mainly by inhibiting osteoclast formation and maturation, but enhanced at 3 mT by promoting osteoclast apoptosis. Moreover, gene expression of RANK, NFATc1, TRAP, CTSK, BAX, and BAX/BCL-2 was significantly decreased by 0.5 mT PEMF, but increased by 3 mT. Our findings reveal a significant intensity window for low-intensity PEMF in regulating bone resorption with diverse nature for modulating osteoclastogenesis and apoptosis. This study not only enriches our basic knowledge for the regulation of PEMF in osteoclastogenesis, but also may lead to more efficient and scientific clinical application of PEMF in regulating bone turnover and inhibiting osteopenia/osteoporosis. Bioelectromagnetics. 38:602-612, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Differential intensity‐dependent effects of pulsed electromagnetic fields on RANKL‐induced osteoclast formation, apoptosis, and bone resorbing ability in RAW264.7 cells

Wang

Liu

Yang

et al. 2017

Bioelectromagnetics

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“…In certain bone modeling phases, ROS may activate osteoclasts while inhibiting osteoblasts [63]. By inducing ROS, ELF-PEMF thus may favor osteoclastogenesis, an assumption supported by the studies of Pi and Zhang [64,65]. However, there are also several other reports showing ELF-PEMF inhibitory effects on osteoclastogenesis [66][67][68].…”

Section: Elf-pemf Effects On Bone Cell Functionmentioning

confidence: 90%

Translational Insights into Extremely Low Frequency Pulsed Electromagnetic Fields (ELF-PEMFs) for Bone Regeneration after Trauma and Orthopedic Surgery

Ehnert

Schröter

Aspera-Werz

et al. 2019

JCM

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The finding that alterations in electrical potential play an important role in the mechanical stimulation of the bone provoked hype that noninvasive extremely low frequency pulsed electromagnetic fields (ELF-PEMF) can be used to support healing of bone and osteochondral defects. This resulted in the development of many ELF-PEMF devices for clinical use. Due to the resulting diversity of the ELF-PEMF characteristics regarding treatment regimen, and reported results, exposure to ELF-PEMFs is generally not among the guidelines to treat bone and osteochondral defects. Notwithstanding, here we show that there is strong evidence for ELF-PEMF treatment. We give a short, confined overview of in vitro studies investigating effects of ELF-PEMF treatment on bone cells, highlighting likely mechanisms. Subsequently, we summarize prospective and blinded studies, investigating the effect of ELF-PEMF treatment on acute bone fractures and bone fracture non-unions, osteotomies, spinal fusion, osteoporosis, and osteoarthritis. Although these studies favor the use of ELF-PEMF treatment, they likewise demonstrate the need for more defined and better controlled/monitored treatment modalities. However, to establish indication-oriented treatment regimen, profound knowledge of the underlying mechanisms in the sense of cellular pathways/events triggered is required, highlighting the need for more systematic studies to unravel optimal treatment conditions.

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“…Arai et al demonstrated that TRAF-mediated Beclin-1 ubiquitination is necessary for RANKL-stimulated osteoclast differentiation, and Beclin-1 knockdown in mice led to the thickening of the cortical bone due to impaired bone resorption [ 57 ]. One of the main signaling pathways involved in the RANKL/RANK system is Ca 2+ -calcineurin-NFATc1 [ 85 ]. The influx of Ca 2+ is essential for osteoclastogenesis and it is mediated by a Ca 2+ -permeable channel named TRPV4 (Transient receptor potential vanilloid 4) [ 86 ].…”

Section: Autophagy In Osteoclast Differentiation/functionmentioning

confidence: 99%

The Role of Autophagy in Osteoclast Differentiation and Bone Resorption Function

et al. 2020

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Autophagy is an evolutionary conserved and highly regulated recycling process of cellular wastes. Having a housekeeping role, autophagy through the digestion of domestic cytosolic organelles, proteins, macromolecules, and pathogens, eliminates unnecessary materials and provides nutrients and energy for cell survival and maintenance. The critical role of autophagy and autophagy-related proteins in osteoclast differentiation, bone resorption, and maintenance of bone homeostasis has previously been reported. Increasing evidence reveals that autophagy dysregulation leads to alteration of osteoclast function and enhanced bone loss, which is associated with the onset and progression of osteoporosis. In this review, we briefly consolidate the current state-of-the-art technology regarding the role of autophagy in osteoclast function in both physiologic and pathologic conditions to have a more general view on this issue.

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Pulsed electromagnetic field inhibits RANKL-dependent osteoclastic differentiation in RAW264.7 cells through the Ca 2+ -calcineurin-NFATc1 signaling pathway

Cited by 26 publications

References 34 publications

Differential intensity‐dependent effects of pulsed electromagnetic fields on RANKL‐induced osteoclast formation, apoptosis, and bone resorbing ability in RAW264.7 cells

Differential intensity‐dependent effects of pulsed electromagnetic fields on RANKL‐induced osteoclast formation, apoptosis, and bone resorbing ability in RAW264.7 cells

Translational Insights into Extremely Low Frequency Pulsed Electromagnetic Fields (ELF-PEMFs) for Bone Regeneration after Trauma and Orthopedic Surgery

The Role of Autophagy in Osteoclast Differentiation and Bone Resorption Function

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