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Introduction
Published in Yufeng Zheng, Magnesium Alloys as Degradable Biomaterials, 2015
In addition, the influence of Mg ions on vascular endothelial cells, embryonic stem cells, adult stem cells, osteoblasts, and osteoclasts are all reported. Maier et al. (2004) reported that a supplement of Mg ions ranging from 2.0 mM to 10.0 mM has a positive effect on the proliferation of human umbilical vein endothelial cells. What's more, the expression of nitric oxide synthase is enhanced at a high Mg ion content. Nguyen et al. (2013) illustrated that embryonic stem cells could tolerate a Mg content of 10 mM, under which the proliferation of embryonic stem cells would not be affected. They also reported a pH limit of 8.1 for culture medium. Shimaya et al. (2010) found that Mg ions with a concentration of 10 mM could add an extracellular matrix of SMSCs and promote differentiation to cartilage cells through activation of some integrin-related signal pathways. Recently, Dai's group reported a strong inhibition of RANKL-induced osteoclast differentiation caused by Mg degradation products (Zhai et al. 2014). They also confirmed that the inhibition process is achieved by inhibition of NF-kappaB and NFATc1 signal pathways.
Osteoimmunomodulation with Biomaterials
Published in Nihal Engin Vrana, Biomaterials and Immune Response, 2018
Bengü Aktaş, Bora Garipcan, Zehra Betül Ahi, Kadriye Tuzlakoğlu, Emre Ergene, Pınar Yılgör Huri
Current studies show that the interactions between these two interrelated systems go beyond the actions of RANKL, including the activity of osteoblasts in maintaining the HSC niche [38,39] and the functions of immune cells in osteoblast and osteoclast development. A number of molecules including cytokines, receptors and transcription factors have been identified as common regulators of both skeletal and immune systems [40,41]. As such, it is well established that M-CSF acts in the regulation of osteoclast differentiation together with RANKL, while a mutation in the corresponding gene for M-CSF negatively affects the development of osteoclasts and macrophages [42]. Insight into the roles of several other factors have been assessed by genetically modified animal models of inflammatory bone loss. For example, mutation in the interferon (IFN)γR1 receptor enhanced bone resorption mediated by osteoclasts [37]. This implies that IFN-γ produced by T-cells blocks osteoclast differentiation. In another study, it was shown that nuclear factor of activated T cells 1 (NFATc1) was essential for osteoclast differentiation both in vitro and in vivo [43]. Altering the levels of NFATcl has been stated as a promising way of decreasing the extent of osteoclast-mediated bone degradation [43]. Similarly, when mutations were made to the bone-related regulatory molecules, alterations in the immunological phenotype were observed in animal and clinical models [44]. For example, when the Spp1 gene responsible for osteopontin production was knocked down, it was observed that fewer natural killer (NK) T-cells were produced by the animal [45]. Several other cytokines, including the interleukin (IL) group have been shown to affect bone metabolism. For example, osteoblast production was encouraged by IL-18 secreted by macrophages, where secretion of IL-1, IL-4 and IL-6 by the T-cells influenced osteoclast formation [46,47].
The application of nanogenerators and piezoelectricity in osteogenesis
Published in Science and Technology of Advanced Materials, 2019
Fu-Cheng Kao, Ping-Yeh Chiu, Tsung-Ting Tsai, Zong-Hong Lin
Bone, as a mechanosensitive organ, reacts to mechanical strain via a series of cytokines and signaling crosstalk between them. Bone remodeling happens after fracture healing and also in each moment whenever bone is dynamically compressed during normal activity, as it is a lifelong process to keep bone tissue at homeostasis. There are two different mechanisms for bone remodeling: the cellular response of osteoblasts and osteoclasts to several key cytokines, and the electrochemical process due to the generation of piezoelectric dipoles. These processes are usually coupled because the piezoelectric potential produced by the deformation of bone tissue can influence the activity of osteocytes inside the bone matrix. The osteocytes can sense the mechanical force via their processes in the canaliculi and then produce several cytokines to regulate osteoclast-mediated bone resorption and osteoblast-mediated bone formation [6,24]. The piezoelectricity induced by mechanical deformation of bone generates a negative electrical charge in areas of bone compression and a positive charge in the areas of traction [25] (Figure 3). The ion channels of the osteocytes can be activated in response to both mechanical stimuli and piezoelectric currents, resulting in hyperpolarization (in the area of a negative charge) or depolarization (in the area of a positive charge) of the plasma membrane [26]. Hyperpolarization of the cell membrane potential promotes osteogenesis and osteogenic differentiation of bone marrow stem cells due to Ras activation, resulting in induction of nuclear osteogenic transcription factor, collagen type I mRNA expression, osteocalcin mRNA expression, and terminal bone matrix deposition [27,28]. RANK (receptor activator of nuclear factor kappa B) is known to play a critical role in osteoclastogenesis [29], and membrane depolarization and Ca2+ influx can lead to the activation and expression of nuclear factor kappa B (NF-κB) [30]. Activated NF-κB stimulates the key osteoclastogenesis regulator, the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1). Subsequently, NFATc1 induces numerous osteoclast-specific target genes that are responsible for cell fusion and function after it translocates into the nucleus [31].