Abstract
Skin is constantly exposed to environmental factors such as pollutants, chemicals and ultra violet radiation (UV), which can induce premature skin aging and increase the risk of skin cancer. One strategy to reduce the effect of oxidative stress produced by environmental exposure is the application of antioxidant molecules. Among the endogenous antioxidants, selenoproteins play a key role in antioxidant defense and in maintaining a reduced cellular environment. Selenium, essential for the activity of selenoproteins, is a trace element that is not synthesized by organisms and must be supplied by diet or supplementation. The aim of this study is to evaluate the effect of Selenium supplementation on skin aging, especially on keratinocytes, the main cells of the epidermis. Our results demonstrate for the first time to our knowledge, the major role of Selenium on the replicative life span of keratinocytes and on aging skin. Selenium protects keratinocyte stem cells (KSCs) against senescence via preservation of their stemness phenotype through adhesion to the basement membrane. Additionally, Selenium supplementation maintains the homeostasis of skin during chronological aging in our senescent skin equivalent model. Controlled supplementation with Selenium could be a new strategy to protect skin against aging.
Highlights
The skin, like every organ and tissue of the human body, is prone to aging
Our results show for the first time that a low-dose Selenium supplement has beneficial effects on keratinocyte stemness and delays skin aging
A portion of our results highlights the positive effect of Selenium on the proliferative properties of keratinocytes and their capacity to give rise to holoclones in culture and their ability to enhance their replicative life span in a monolayer culture
Summary
The skin, like every organ and tissue of the human body, is prone to aging. the skin aging process is affected by both intrinsic and extrinsic factors. Skin is composed of a pluristratified epidermis firmly anchored to the dermis through a complex structure, the dermal epidermal junction (DEJ) Aging impacts both the epidermal and dermal parts of the skin, with a progressive loss of homeostasis, especially in the balance between proliferation and differentiation of the epidermis [1] and in the loss of interaction between the dermis and epidermis via disorganization of the DEJ [2]. Keratinocyte stem cells (KSCs) are necessary to ensure constant renewal www.aging‐us.com of the epidermis throughout life. They are maintained and protected as stem cells in a microenvironment called a “niche” and are strongly anchored to the DEJ through β1 and α6 integrin binding to type IV collagen and laminin 332, respectively, the main components of the basement membrane [3,4]. KSCs interactions with the DEJ are crucial for stemness, homeostasis, and skin structural integrity
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