Epidermal iron metabolism for iron salvage

Asano, Masayuki; Yamasaki, Kenshi; Yamauchi, Takashi; Terada, Tadashi; Aiba, Setsuya

doi:10.1016/j.jdermsci.2017.04.003

Cited by 12 publications

(24 citation statements)

References 29 publications

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“…We observed a significant Cu signal with a distinct distribution pattern (Figure 3 and Figure S2A,B). 56 Fe showed an inverse distribution pattern relative to Ca in our study, again in agreement with previous reports 21 . Although there is no report of Ba and Sr in human skin to our knowledge, we detected these elements in all samples with distinct distribution patterns.…”

Section: Discussionsupporting

confidence: 93%

“…56 Fe showed an inverse distribution pattern relative to Ca in our study, again in agreement with previous reports. 21 Although there is no report of Ba and Sr in human skin to our knowledge, we detected these elements in all samples with distinct distribution patterns. The 138 Ba and 88 Sr signal patterns seem similar to those 64 Zn, 31 P, 39 K, 23 Na, 34 S, 63 Cu, and 24 Mg. Mo has been detected in several organs, and Mo-dependent enzymes are known.…”

Section: Discussioncontrasting

confidence: 50%

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Comprehensive analysis of elemental distribution in human skin using laser ablation inductively coupled plasma mass spectrometry

Nakanishi

Kamezono

Nakatani

et al. 2020

Skin Research and Technology

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The amounts and distributions of chemical elements in skin are important to maintain homeostasis. For example, gradients of Ca, K, and Mg have been well investigated and play roles in keratinocyte differentiation and water-impermeable barrier homeostasis. [1][2][3][4] These gradients are disrupted after barrier disruption or in patients with diseases associated with barrier dysfunction, such as psoriasis or atopic dermatitis. [4][5][6] Furthermore, Zn, Cu, Fe, and Mn in keratinocytes are involved in wound healing, 7-10 while Se has a role in protection against ultraviolet radiation (UV). 11 Several reports have suggested that Zn and Sr might be associated cutaneous pruritus. 12-14 Therefore, observation of the amounts and distributions of chemical elements in the skin can give us important information about skin pathology. So far, X-ray microanalysis methods, such as electron-probe X-ray microanalysis (XRMA) and particle-induced X-ray emission (PIXE), and fluorescence microscopy using chemical indicators have been used for this purpose. [4][5][6]15,16 However, XRMA

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Section: Discussionsupporting

confidence: 93%

Section: Discussioncontrasting

confidence: 50%

Comprehensive analysis of elemental distribution in human skin using laser ablation inductively coupled plasma mass spectrometry

Nakanishi

Kamezono

Nakatani

et al. 2020

Skin Research and Technology

View full text Add to dashboard Cite

show abstract

“…We also show that iron sequestration, which mimics hypoxia and induces mitophagy (Allen et al, 2013), increases NIX expression and promotes mitochondrial fragmentation. It will be interesting in future studies to determine whether the epidermis contributes to iron homeostasis via mitophagy, which could help the body reclaim mitochondrial iron prior to corneocyte shedding (Asano et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

NIX initiates mitochondrial fragmentation via DRP1 to drive epidermal differentiation

et al. 2021

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SUMMARY The epidermis regenerates continually to maintain a protective barrier at the body’s surface composed of differentiating keratinocytes. Maturation of this stratified tissue requires that keratinocytes undergo wholesale organelle degradation upon reaching the outermost tissue layers to form compacted, anucleate cells. Through live imaging of organotypic cultures of human epidermis, we find that regulated breakdown of mitochondria is critical for epidermal development. Keratinocytes in the upper layers initiate mitochondrial fragmentation, depolarization, and acidification upon upregulating the mitochondrion-tethered autophagy receptor NIX. Depleting NIX compromises epidermal maturation and impairs mitochondrial elimination, whereas ectopic NIX expression accelerates keratinocyte differentiation and induces premature mitochondrial fragmentation via the guanosine triphosphatase (GTPase) DRP1. We further demonstrate that inhibiting DRP1 blocks NIX-mediated mitochondrial breakdown and disrupts epidermal development. Our findings establish mitochondrial degradation as a key step in terminal keratinocyte differentiation and define a pathway operating via the mitophagy receptor NIX in concert with DRP1 to drive epidermal morphogenesis.

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“…It is known that for rapid proliferation, cells enhance metabolic activity allowing for increased DNA biosynthesis; this may describe why HaCaT cells to have high iron levels and require less ferritin. However, in SiHa, oxidative stress may be controlled through maintaining lower free iron levels, as intracellular iron may be harmful due to its ability to produce ROS (37–40).…”

Section: Discussionmentioning

confidence: 99%

17β‑estradiol‑induced mitochondrial dysfunction and Warburg effect in cervical cancer cells allow cell survival under metabolic stress

et al. 2019

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Mitochondria from different types of cancer show bioenergetics and dysfunction that favor cell proliferation. The mechanistic understanding of estrogen in cervical cancer is poorly understood. Therefore, the objective of this study was to determine how 17β-estradiol (E2) affects mitochondrial function and the Warburg effect in SiHa, HeLa and C33A cervical cancer cells. Mitochondrial compromise was evaluated measuring changes in the membrane permeability by immunofluorescence, calcium concentration, redox status, iron and ferritin reserves. Glucose consumption and lactic acid assays were used to detect the metabolic activity. Results were confirmed at molecular level by analysis of the differential gene expression using RNA sequencing. E2 modified the mitochondrial permeability and produced an alteration in the calcium signaling pathway. In HeLa and SiHa, there was a significant decrease in nitric oxide levels and lipid peroxidation, and an increase in glucose consumption and lactic acid levels when stimulated with E2. Intracellular iron or ferritin reserves were not affected by the E2 treatment. Genes differentially modulated by E2 were involved in the mitochondrial electron transport chain, oxidative phosphorylation system, glycolysis, pentose phosphate pathway and the regulation of metabolic signaling pathways. Herein, we provide evidence for a primary effect of estrogen on mitochondrial function and the Warburg effect, favoring the metabolic adaptation of the cervical cancer cell lines and their survival.

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Epidermal iron metabolism for iron salvage

Abstract: These studies demonstrated that the epidermis is equipped with a machinery by which intracellular iron in differentiated keratinocytes is excreted to the extracellular space before reaching the stratum corneum.

Cited by 12 publications

References 29 publications

Comprehensive analysis of elemental distribution in human skin using laser ablation inductively coupled plasma mass spectrometry

Comprehensive analysis of elemental distribution in human skin using laser ablation inductively coupled plasma mass spectrometry

NIX initiates mitochondrial fragmentation via DRP1 to drive epidermal differentiation

17β‑estradiol‑induced mitochondrial dysfunction and Warburg effect in cervical cancer cells allow cell survival under metabolic stress

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