Ferric ion could facilitate osteoclast differentiation and bone resorption through the production of reactive oxygen species

Jia, Peng; Xu, You Sheng; Zhang, Zeng Li; Li, Kai; Li, Bingyan; Zhang, Wen; Yang, Huilin

doi:10.1002/jor.22133

Cited by 117 publications

(84 citation statements)

References 42 publications

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“…In other words, excess iron promoted the activity of osteoclasts, and then elevated bone resorption process, with resultant loss of bone strength. In terms of the molecular mechanisms, previous studies have demonstrated that intracellular iron retention would cause massive production of reactive oxygen species (ROS) through Fenton reaction (Fridovich, 1978;Galaris and Pantopoulos, 2008;Halliwell and Gutteridge, 1990), and ROS is postulated to be an instigator of bone resorption (Jia et al, 2012). Jia and colleagues demonstrated that iron overload could promote osteoclast differentiation and bone resorption through stimulation of ROS (Ishii et al, 2009;Yamasaki and Hagiwara, 2009).…”

Section: Discussionmentioning

confidence: 99%

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Sun

Guo

Yin

et al. 2014

Gene

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Osteoporosis is one of the leading disorders among aged people. Bone loss results from a number of physiological alterations, such as estrogen decline and aging. Meanwhile, iron overload has been recognized as a risk factor for bone loss. Systemic iron homeostasis is fundamentally governed by the hepcidin-ferroportin regulatory axis, where hepcidin is the key regulator. Hepcidin deficiency could induce a few disorders, of which iron overload is the most representative phenotype. However, there was little investigation of the effects of hepcidin deficiency on bone metabolism. To this end, hepcidin-deficient (Hamp1 −/− ) mice were employed to address this issue. Our results revealed that significant iron overload was induced in Hamp1 −/− mice. Importantly, significant decreases of maximal loading and maximal bending stress were found in Hamp1 −/− mice relative to wildtype (WT) mice.Moreover, the levels of the C-telopeptide of type I collagen (CTX-1) increased in Hamp1 −/− mice. Therefore, hepcidin deficiency resulted in a marked reduction of bone load-bearing capacity likely through enhancing bone resorption, suggesting a direct correlation between hepcidin deficiency and bone loss. Targeting hepcidin or the pathway it modulates may thus represent a therapeutic for osteopenia or osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Sun

Guo

Yin

et al. 2014

Gene

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“…In osteoclasts, iron excess stimulates osteoclastogenesis by supporting mitochondrial respiration, [18][19][20] while sequestering iron from osteoclasts inhibits their maturation and function. [21][22] In contrast, osteoblast function is suppressed by iron excess in osteoblast cell lines, [23][24][25] while iron chelation using deferoxamine (DFO) seems to exert positive effects on osteoblast maturation.…”

Section: Introductionmentioning

confidence: 99%

Wnt5a is a key target for the pro-osteogenic effects of iron chelation on osteoblast progenitors

et al. 2016

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“…67 Moreover, ferric ionic state successfully promoted Schwann cell and osteoclast differentiation. 68,69 These phenomena may help explain why transferrin and ferric ions play indispensable roles in driving motor neuron differentiation.…”

Section: Discussionmentioning

confidence: 99%

Accelerated Neuronal Differentiation Toward Motor Neuron Lineage from Human Embryonic Stem Cell Line (H9)

Chen

Lee

et al. 2015

Tissue Engineering Part C: Methods

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Motor neurons loss plays a pivotal role in the pathoetiology of various debilitating diseases such as, but not limited to, amyotrophic lateral sclerosis, primary lateral sclerosis, progressive muscular atrophy, progressive bulbar palsy, pseudobulbar palsy, and spinal muscular atrophy. However, advancement in motor neuron replacement therapy has been significantly constrained by the difficulties in large-scale production at a costeffective manner. Current methods to derive motor neuron heavily rely on biochemical stimulation, chemical biological screening, and complex physical cues. These existing methods are seriously challenged by extensive time requirements and poor yields. An innovative approach that overcomes prior hurdles and enhances the rate of successful motor neuron transplantation in patients is of critical demand. Iron, a trace element, is indispensable for the normal development and function of the central nervous system. Whether ferric ions promote neuronal differentiation and subsequently promote motor neuron lineage has never been considered. Here, we demonstrate that elevated iron concentration can drastically accelerate the differentiation of human embryonic stem cells (hESCs) toward motor neuron lineage potentially via a transferrin mediated pathway. HB9 expression in 500 nM iron-treated hESCs is approximately twofold higher than the control. Moreover, iron treatment generated more matured and functional motor neuron-like cells that are *1.5 times more sensitive to depolarization when compared to the control. Our methodology renders an expedited approach to harvest motor neuron-like cells for disease, traumatic injury regeneration, and drug screening.

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Ferric ion could facilitate osteoclast differentiation and bone resorption through the production of reactive oxygen species

Cited by 117 publications

References 42 publications

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Hepcidin deficiency undermines bone load-bearing capacity through inducing iron overload

Wnt5a is a key target for the pro-osteogenic effects of iron chelation on osteoblast progenitors

Accelerated Neuronal Differentiation Toward Motor Neuron Lineage from Human Embryonic Stem Cell Line (H9)

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