Abstract
The outer epidermal skin is a primary barrier that protects the body from extrinsic factors, such as ultraviolet (UV) radiation, chemicals and pollutants. The complete epithelialization of a wound by keratinocytes is essential for restoring the barrier function of the skin. However, age-related alterations predispose the elderly to impaired wound healing. Therefore, wound-healing efficacy could be also considered as a potent function of an anti-aging reagent. Here, we examine the epidermal wound-healing efficacy of the fourth-generation retinoid, seletinoid G, using HaCaT keratinocytes and skin tissues. We found that seletinoid G promoted the proliferation and migration of keratinocytes in scratch assays and time-lapse imaging. It also increased the gene expression levels of several keratinocyte proliferation-regulating factors. In human skin equivalents, seletinoid G accelerated epidermal wound closure, as assessed using optical coherence tomography (OCT) imaging. Moreover, second harmonic generation (SHG) imaging revealed that seletinoid G recovered the reduced dermal collagen deposition seen in ultraviolet B (UVB)-irradiated human skin equivalents. Taken together, these results indicate that seletinoid G protects the skin barrier by accelerating wound healing in the epidermis and by repairing collagen deficiency in the dermis. Thus, seletinoid G could be a potent anti-aging agent for protecting the skin barrier.
Highlights
The skin, which comprises the outer epidermis, underlying connective tissue and the dermis, functions as a barrier that protects the body from environmental stressors, such as pathogens and physical stress [1]
Aged skin is more prone to injury, and scars formed by aged skin are weaker than those formed by younger skin
Studies on the relationship between aging and wound-healing processes have indicated that the altered mechanical environment of aged skin may largely account for age-related delays in healing [5,6,7]
Summary
The skin, which comprises the outer epidermis, underlying connective tissue and the dermis, functions as a barrier that protects the body from environmental stressors, such as pathogens and physical stress [1]. Skin injuries may damage the epidermis and dermal layers, necessitating repair through wound-healing processes, such as proliferation and re-epithelialization [2]. When this well-ordered process is disrupted, as can be seen with age, the injury may develop into a chronic wound [3,4]. Studies have shown that seletinoid G repairs altered connective tissue in old skin [12], promotes adiponectin production during adipogenesis [14], stimulates adiponectin-induced hair growth factors in human dermal papilla cells [15], dually modulates peroxisome proliferator-activated receptor α/γ (PPARα/γ) and inhibits ultraviolet B (UVB) irradiation-induced inflammation in human epidermal keratinocytes [16]. Three-dimensional investigation using second harmonic generation (SHG) imaging was used to reveal that seletinoid G realigns collagen deposition in the dermis of human skin equivalents
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