Iron metabolism gene expression in human skeletal muscle

Polonifi, Aikaterini; Politou, Marianna; Kalotychou, Vasiliki; Xiromeritis, Konstantinos; Tsironi, Maria; Berdoukas, Vasileios; Vaiopoulos, G; Aessopos, Athanasios

doi:10.1016/j.bcmd.2010.07.002

Cited by 16 publications

(15 citation statements)

References 44 publications

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“…Similar results were found when human skeletal muscle cells were exposed to iron, where genes involved in iron homeostasis were found to be considerably regulated [25]. We also observed that some iron homeostasis genes were regulated when exposed to the alloy, although their levels of change in expression did not satisfy the cut-off value fixed to be considered as significant.…”

Section: Discussionsupporting

confidence: 71%

Gene expression profile of mouse fibroblasts exposed to a biodegradable iron alloy for stents

et al. 2013

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Iron based materials could constitute an interesting option for cardiovascular biodegradable stent applications due to their superior ductility compared to their counterparts-magnesium alloys. Since the predicted degradation rate of pure iron is considered slow, manganese (35% w/w), an alloying element for iron, was explored to counteract this problem through the powder metallurgy process . However, manganese presents a high cytotoxic potential, thus its effect on cells must first be established. Here, we explored a new method to investigate a degradable metallic material (DMM) by establishing the gene expression profile (GEP) of mouse 3T3 fibroblasts exposed to Fe-35Mn degradation products in order to better understand cell response to potentially cytotoxic DMM. Briefly, 3T3 cells were exposed to degradation products eluting through tissue culture insert filter (3 µm pore size) containing cytostatic amounts of 3.25 mg/ml of Fe-35Mn powder, 0,25 mg/ml of pure Mn powder or 5 mg/ml of pure iron powder for 24 hours. We then conducted a gene expression profiling study from these cells. Exposure of 3T3 cells to Fe-35Mn was associated with the up-regulation of 75 genes and down-regulation of 59 genes, while 126 were up-regulated and 76 down-regulated genes in presence of manganese. No genes were found regulated for the iron powder. When comparing the GEP of 3T3 fibroblasts in presence of Fe-35Mn and Mn, 68 up-regulated and 54 down-regulated genes were common. These results were confirmed by quantitative RT-PCR for a subset of these genes. This GEP study could provide clues about the mechanism behind degradation products effects on cells of the Fe-35Mn alloy and may help in the appraisal of its potential for DMM applications.

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Section: Discussionsupporting

confidence: 71%

Gene expression profile of mouse fibroblasts exposed to a biodegradable iron alloy for stents

et al. 2013

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“…For example, Polonifi et al examined skeletal muscle iron metabolism and confirmed the expression of several genes implicated in four pathways: iron import, export, storage, and regulation (for a detailed review of iron metabolism genes in skeletal muscle, see Polonifi et al and Sekyere et al ) As mentioned before, little has as yet been unravelled regarding the mechanisms that control local iron regulation in skeletal muscle. Since the expression of two main regulatory peptides, namely HAMP and HJV, has been confirmed in skeletal muscle, the existence of tissue‐specific translational iron regulation can be assumed. Although the production of HAMP in skeletal muscle is negligible (in comparison with hepatic production), some preliminary results indicate its potential contribution to local iron regulation and immune response .…”

Section: Critical Role Of Optimal Iron Availability For Effective Celmentioning

confidence: 94%

The influence of iron deficiency on the functioning of skeletal muscles: experimental evidence and clinical implications

Stugiewicz

Tkaczyszyn

Kasztura

et al. 2016

European J of Heart Fail

123

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Skeletal and respiratory myopathy not only constitutes an important pathophysiological feature of heart failure and chronic obstructive pulmonary disease, but also contributes to debilitating symptomatology and predicts worse outcomes in these patients. Accumulated evidence from laboratory experiments, animal models, and interventional studies in sports medicine suggests that undisturbed systemic iron homeostasis significantly contributes to the effective functioning of skeletal muscles. In this review, we discuss the role of iron status for the functioning of skeletal muscle tissue, and highlight iron deficiency as an emerging therapeutic target in chronic diseases accompanied by a marked muscle dysfunction.

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“…It is the ratio of membrane GPI-linked HJV to soluble HJV that determines the concentration of hepcidin through this pathway (Babitt et al, 2007). In fact, profiling of iron metabolism genes in human skeletal muscle and liver under physiological conditions revealed that HJV expression is higher in skeletal muscle relative to the liver (Polonifi et al, 2010). This is of note, especially because of the high levels of HJV and hepcidin found in the liver of MCK-Fxn-KO (Whitnall et al, 2012), pointing to a direct influence of frataxin on systemic iron metabolism.…”

Section: Frataxin Deficiency In Cardiac and Skeletal Muscle Affects Smentioning

confidence: 99%

Fixing frataxin: ‘ironing out’ the metabolic defect in Friedreich's ataxia

Anzovino

Lane

Huang

et al. 2014

British J Pharmacology

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The metabolically active and redox-active mitochondrion appears to play a major role in the cellular metabolism of the transition metal, iron. Frataxin, a mitochondrial matrix protein, has been identified as playing a key role in the iron metabolism of this organelle due to its iron-binding properties and is known to be essential for iron-sulphur cluster formation. However, the precise function of frataxin remains elusive. The decrease in frataxin expression, as seen in the inherited disorder Friedreich's ataxia, markedly alters cellular and mitochondrial iron metabolism in both the mitochondrion and the cell. The resulting dysregulation of iron trafficking damages affects tissues leading to neuro-and cardiodegeneration. This disease underscores the importance of iron homeostasis in the redox-active environment of the mitochondrion and the molecular players involved. Unravelling the mechanisms of altered iron metabolism in Friedreich's ataxia will help elucidate a biochemical function for frataxin. Consequently, this will enable the development of more effective and rationally designed treatments. This review will focus on the emerging function of frataxin in relation to the observed alterations in mitochondrial iron metabolism in Friedreich's ataxia. Tissue-specific alterations due to frataxin loss will also be discussed, as well as current and emerging therapeutic strategies.

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Iron metabolism gene expression in human skeletal muscle

Cited by 16 publications

References 44 publications

Gene expression profile of mouse fibroblasts exposed to a biodegradable iron alloy for stents

Gene expression profile of mouse fibroblasts exposed to a biodegradable iron alloy for stents

The influence of iron deficiency on the functioning of skeletal muscles: experimental evidence and clinical implications

Fixing frataxin: ‘ironing out’ the metabolic defect in Friedreich's ataxia

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