Involvement of changes in stratum corneum keratin in wrinkle formation by chronic ultraviolet irradiation in hairless mice

Abstract

Chronic exposure to ultraviolet (UV) radiation alters components of the skin. We previously reported that chronic low-dose UV irradiation induced wrinkle formation but did not significantly alter dermal components of hairless mice. In the present study, we examined whether the epidermal changes by UV irradiation could contribute to wrinkle formation. Hairless mice were irradiated with one-third the minimum erythema dose (MED) of UVB (20 mJ/cm2) and UVA (14 J/cm2) for 10 weeks, and followed up for another 24weeks without irradiation. Fine wrinkles were detected following irradiation, which existed even 24 weeks after cessation of irradiation. An increase in the viscoelastic proportion of the total distension (Uv/Ue) was recognized in irradiated mice, which may be related to wrinkle formation. In the epidermis, an increase in the amount of transepidermal water loss and a decrease in the water content of the stratum corneum were seen after 10 weeks of UV irradiation, neither of which recovered during the 24-week observation period. In addition, there was a significant increase in the amount of stratum corneum keratin after 10 weeks of irradiation, which persisted during the 24-week follow-up. The results of our study suggest that chronic low-dose UV irradiation primarily alters the epidermal rather than the dermal components of the skin. In addition, our results indicate that the increased keratin content of the stratum corneum may be involved in the alteration of the physical properties of the skin. This process could be one of the early events of wrinkle formation.

Mechanistic Effects of Long-Term Ultraviolet B Irradiation Induce Epidermal and Dermal Changes in Human Skin Xenografts

“…Previous studies in animal models indicate the cause effect relationship between repetitive UV irradiation and an increase of keratins K1, K5, and K10, with no changes in the collagen fibers and elastic fibers, resulting in loss of skin elasticity and the formation of skin wrinkles. 12,13 Conversely, in our study, repeated UVB irradiation stimulated a stable expression of keratins K6 and its partners K16 and K17, but not K1, K5, and K10. Keratins K6, K16, and/or K17, which are not usually expressed in the innate state of normal epidermis, have been reported to initially induce in the suprabasal layers as early as 6 hours after injury or during the first 24 to 48 hours of UVB irradiation.…”

“…[1][2][3] Skin photodamage is physiologically correlated with several alterations including the increase and disorganization of elastic fibers and the reduction of collagens in the dermal extracellular matrix 4 -11 and the increase of keratin contents and the deterioration of keratin intermediate filaments (KIFs) in the epidermis. [12][13][14] Elastic fibers are age-dependent-decreasing dermal extracellular matrix that respond primarily to the fibrous mechanism controlling cutaneous elasticity. 4,5,15,16 The accumulation of dystrophic elastotic material in the reticular dermis, referred to as solar elastosis, is commonly observed in photoaged skin.…”

“…38 -41 In hairless mice, a repeated low-dose UV exposure has been reported to deteriorate KIFs and induce the expression of epithelial keratins (K1, K5, and K10), resulting in the loss of skin elasticity and eventually initiating wrinkled skin, consistent with previous reports demonstrating no causal relationship between wrinkle formation and dermal changes. [12][13][14]42,43 Many studies of skin photoaging have been conducted using animal models and human skin substitute. The results may be misleading because of inferior architecture, such as the relative thin epidermal layer and compromised barrier function.…”

Solar UV radiation reduces the barrier function of human skin

“…Recent in vivo studies have shown that UVB radiation affects epidermal morphology, including increasing the mean SC thickness (12), and disrupts the permeability barrier, causing morphological changes in SC lipids, increased transepidermal water loss, and decreased SC hydration (13,14). Surprisingly, to our knowledge, no studies have explored how UV exposure affects the mechanical barrier function of SC.…”

Non-melanoma Skin Cancer in Canada Chapter 2: Primary Prevention of Non-melanoma Skin Cancer

“…29 UVB also alters skin lipid composition and enzyme metabolism, 30,31 increasing transepidermal water loss. 31,32 These events culminate in premature aging of the skin, such as actinic elastosis.…”