Abstract
Skin aging involves genetic, environmental and hormonal factors.Facial wrinkles also depend on muscular activity. Gene expression investigation may be useful for new anti-aging products. To evaluate structure and gene expression differences among exposed and unexposed skin in menopausal women. Cross-sectional study, including 15 menopausal women, 55-65 years, phototype III; photo-exposed, periorbital wrinkles (A1), preauricular, not wrinkled (A2), and unexposed gluteal (A3) areas were described and compared by non-invasive measures, histology, immunohistochemistry and gene expression (RNASeq); participants mean age was 61yo, presenting moderate periorbital wrinkles and light facial photodamage. Higher roughness, wrinkles number and echogenicity were observed in A1 and A2 versus A3. Decreased epidermal thickness and dermal collagen IV were demonstrated in A1 versus A2 and A3. Exposed areas impacted different pathways compared to unexposed. Exposed wrinkled skin (A1) showed impact on cell movement with decreased inflammatory activation state. Pathways related to lipid and aminoacids metabolism were modulated in non-wrinkled exposed (A2) compared to unexposed (A3) skin. Expected histological findings and gene expression differences among areas were observed. Photoaging in menopausal women may modulate lipid and aminoacids metabolism and decrease inflammatory and keratinization pathways, cellular homeostasis, immune response, fibrogenesis and filament formation. These findings may help development of new therapies for skin health and aging control.
Highlights
Skin aging is a complex biological process caused by intrinsic or genetic and extrinsic or environmental factors [28, 47]
Synthesis of dermal matrix components, especially collagen I and IV and elastin is reduced with concomitant increase in their degradation, by metalloproteinases (MMPs)
The photoaging is the major component of extrinsic aging [20]
Summary
Skin aging is a complex biological process caused by intrinsic or genetic and extrinsic or environmental factors [28, 47]. The superposition of intrinsic and extrinsic aging, named photoaging, is responsible for 85% of aged skin phenotype in exposed areas. The chronic exposure to aggressors like solar radiation, especially ultra-violet (UV), tobacco, pollution and hot climate causing activation of transient receptor potential cation channel subfamily V member 1 (TrpV1), accelerate the skin aging [11, 30]. Clinical signs of aged skin include reduced thickness, hydration and elasticity, with progressive development of sagginess, wrinkles, sulcus, and dyschromia [35], which are more evident and severe in photo-exposed areas of Caucasian population [20]. Antioxidant depletion, lipid peroxidation and decomposition of sebaceous lipids occur [3, 36, 37, 40, 47, 48]
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