Magnesium Supplementation Attenuates Ultraviolet-B-Induced Damage Mediated through Elevation of Polyamine Production in Human HaCaT Keratinocytes

Shu, Shokoku; Kobayashi, Mao; Marunaka, Kana; Yoshino, Yuta; Goto, Makiko; Katsuta, Yuji; Ikari, Akira

doi:10.3390/cells11152268

Cited by 5 publications

(6 citation statements)

References 41 publications

(43 reference statements)

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“…This result suggests that the change in [Mg 2+ ] cyto is a mitochondria-protective mechanism under oxidative stress conditions. Previous studies have also demonstrated the long-term effects of Mg 2+ on cell protection in keratinocytes 42 and other cells 22 , 24 . [Mg 2+ ] cyto changes the activity of phosphatases, such as mTOR, CREB, and ERK 16 , and leads to cell protection under stress conditions in keratinocytes 42 and neurons 22 .…”

Section: Discussionmentioning

confidence: 98%

“…Previous studies have also demonstrated the long-term effects of Mg 2+ on cell protection in keratinocytes 42 and other cells 22 , 24 . [Mg 2+ ] cyto changes the activity of phosphatases, such as mTOR, CREB, and ERK 16 , and leads to cell protection under stress conditions in keratinocytes 42 and neurons 22 . Therefore, Mg 2+ has both acute and long-term protective effects for cells.…”

Section: Discussionmentioning

confidence: 98%

“…This suggest that Mg 2+ acts as a negative feedback signal to maintain ATP level against stress on cells. Some studies have already demonstrated that mitochondria was protected from oxidative stress under Mg 2+ rich conditions, but these studies have not referred to changes in [Mg 2+ ] cyto levels 24 , 27 , 42 . Our data reveal that [Mg 2+ ] cyto increases in response to oxidative stress and that Mg 2+ that dissociated from Mg-ATP is not a byproduct but instead acts as a mechanism to protect the mitochondria.…”

Section: Discussionmentioning

confidence: 99%

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Intracellular Mg2+ protects mitochondria from oxidative stress in human keratinocytes

Fujita,

Shindo,

Katsuta

et al. 2023

Commun Biol

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Reactive oxygen species (ROS) are harmful for the human body, and exposure to ultraviolet irradiation triggers ROS generation. Previous studies have demonstrated that ROS decrease mitochondrial membrane potential (MMP) and that Mg2+ protects mitochondria from oxidative stress. Therefore, we visualized the spatio-temporal dynamics of Mg2+ in keratinocytes (a skin component) in response to H2O2 (a type of ROS) and found that it increased cytosolic Mg2+ levels. H2O2-induced responses in both Mg2+ and ATP were larger in keratinocytes derived from adults than in keratinocytes derived from newborns, and inhibition of mitochondrial ATP synthesis enhanced the H2O2-induced Mg2+ response, indicating that a major source of Mg2+ was dissociation from ATP. Simultaneous imaging of Mg2+ and MMP revealed that larger Mg2+ responses corresponded to lower decreases in MMP in response to H2O2. Moreover, Mg2+ supplementation attenuated H2O2-induced cell death. These suggest the potential of Mg2+ as an active ingredient to protect skin from oxidative stress.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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Intracellular Mg2+ protects mitochondria from oxidative stress in human keratinocytes

Fujita,

Shindo,

Katsuta

et al. 2023

Commun Biol

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“…We reported that Mg 2+ treatment of epidermal keratinocytes increases the expression of hyaluronic acid synthase via glycogen synthase kinase 3 and the cyclic AMP response element binding protein, resulting in increased hyaluronic acid production, which promotes wound healing [19]. We also demonstrated that Mg 2+ treatment increases polyamine synthesis and reduces ultraviolet (UVB)-induced cell death in keratinocytes [20]. The above reports suggest that Mg 2+ treatment may have several beneficial effects on epidermal keratinocytes.…”

Section: Introductionmentioning

confidence: 92%

Unraveling the Mechanisms Involved in the Beneficial Effects of Magnesium Treatment on Skin Wound Healing

Yoshino,

Teruya,

Miyamoto

et al. 2024

IJMS

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The skin wound healing process consists of hemostatic, inflammatory, proliferative, and maturation phases, with a complex cellular response by multiple cell types in the epidermis, dermis, and immune system. Magnesium is a mineral essential for life, and although magnesium treatment promotes cutaneous wound healing, the molecular mechanism and timing of action of the healing process are unknown. This study, using human epidermal-derived HaCaT cells and human normal epidermal keratinocyte cells, was performed to investigate the mechanism involved in the effect of magnesium on wound healing. The expression levels of epidermal differentiation-promoting factors were reduced by MgCl2, suggesting an inhibitory effect on epidermal differentiation in the remodeling stage of the late wound healing process. On the other hand, MgCl2 treatment increased the expression of matrix metalloproteinase-7 (MMP7), a cell migration-promoting factor, and enhanced cell migration via the MEK/ERK pathway activation. The enhancement of cell migration by MgCl2 was inhibited by MMP7 knockdown, suggesting that MgCl2 enhances cell migration which is mediated by increased MMP7 expression. Our results revealed that MgCl2 inhibits epidermal differentiation but promotes cell migration, suggesting that applying magnesium to the early wound healing process could be beneficial.

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“…On the other hand, their catabolism involves the enzymes spermine oxidase (SMOX), spermine-/spermidine-N1-acetyltransferase 1 (SAT1) and polyamine oxidase (PAOX), which, as a whole, regulate PAs homeostasis [ 27 ] ( Figure 1 ). Polyamines, among the other biological functions, act as antioxidants and free radical scavengers, therefore contributing to the oxidative balance of the cell [ 25 , 28 , 29 ].…”

Section: Introductionmentioning

confidence: 99%

The Impact of Spermidine on C2C12 Myoblasts Proliferation, Redox Status and Polyamines Metabolism under H2O2 Exposure

Ceci

Duranti

Giuliani

et al. 2022

IJMS

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A central feature of the skeletal muscle is its ability to regenerate through the activation, by environmental signals, of satellite cells. Once activated, these cells proliferate as myoblasts, and defects in this process profoundly affect the subsequent process of regeneration. High levels of reactive oxygen species such as hydrogen peroxide (H2O2) with the consequent formation of oxidized macromolecules increase myoblasts’ cell death and strongly contribute to the loss of myoblast function. Recently, particular interest has turned towards the beneficial effects on muscle of the naturally occurring polyamine spermidine (Spd). In this work, we tested the hypothesis that Spd, upon oxidative challenge, would restore the compromised myoblasts’ viability and redox status. The effects of Spd in combination with aminoguanidine (Spd-AG), an inhibitor of bovine serum amine oxidase, on murine C2C12 myoblasts treated with a mild dose of H2O2 were evaluated by analyzing: (i) myoblast viability and recovery from wound scratch; (ii) redox status and (iii) polyamine (PAs) metabolism. The treatment of C2C12 myoblasts with Spd-AG increased cell number and accelerated scratch wound closure, while H2O2 exposure caused redox status imbalance and cell death. The combined treatment with Spd-AG showed an antioxidant effect on C2C12 myoblasts, partially restoring cellular total antioxidant capacity, reducing the oxidized glutathione (GSH/GSSG) ratio and increasing cell viability through a reduction in cell death. Moreover, Spd-AG administration counteracted the induction of polyamine catabolic genes and PA content decreased due to H2O2 challenges. In conclusion, our data suggest that Spd treatment has a protective role in skeletal muscle cells by restoring redox balance and promoting recovery from wound scratches, thus making myoblasts able to better cope with an oxidative insult.

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Magnesium Supplementation Attenuates Ultraviolet-B-Induced Damage Mediated through Elevation of Polyamine Production in Human HaCaT Keratinocytes

Cited by 5 publications

References 41 publications

Intracellular Mg2+ protects mitochondria from oxidative stress in human keratinocytes

Intracellular Mg2+ protects mitochondria from oxidative stress in human keratinocytes

Unraveling the Mechanisms Involved in the Beneficial Effects of Magnesium Treatment on Skin Wound Healing

The Impact of Spermidine on C2C12 Myoblasts Proliferation, Redox Status and Polyamines Metabolism under H2O2 Exposure

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