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Background: Visual and molecular changes occurring upon aging are rather well characterized. Still, aging signs show great significant inter‐individual variations, and little is known concerning the link between perceived age and cutaneous microcirculation. Materials and Methods: To investigate this point, we recruited Caucasian women in their mid‐50's to mid‐70's and subsampled women looking older or younger than their age. We studied their facial skin color, as well as their microvascular reactivity to local heating assessed in the forearm skin. We also used skin biopsies from some of these women for gene expression or immunohistochemical analysis. Results: Clinical and instrumental analysis of skin color revealed that subjects who look 5 years younger differ only by a higher glowing complexion. Our most striking result is that subjects looking 5 years younger than their age present a higher microcirculation reactivity in forearm skin. Transcriptome comparison of skin samples from women looking older or younger than their age revealed 123 annotated transcripts differentially expressed, among which MYL9 relates to microcirculation. MYL9 is downregulated in the group of women looking younger than their real age. Microscopy shows that the labeling of MYL9 and CD31 are altered and heterogeneous with age, as is the morphology of microvessels. Conclusion: Therefore, assessing generalized vascular reactivity in non‐photo‐exposed skin to focus on the intrinsic aging allows subtle discrimination of perceived age within elderly healthy subjects. [ABSTRACT FROM AUTHOR]

Thirty-five women were included in a clinical study to characterize the volatile organic compounds (VOCs) emitted by the skin during exposure to psychological stress. An original silicon-based polymeric phase was used for VOC sampling on the forehead before and after stress induction. Cognitive stress was induced using specialized software that included a chronometer for semantic and arithmetic tasks. Assessment of stress was monitored using a State-trait anxiety inventory questionnaire, analysis of participants' verbal expressions and clinical measurements. Identification and relative quantification of VOCs were performed by gas chromatography-mass spectrometry. Stress induction was validated by a significant increase in state-anxiety as indicated by the questionnaire, modifications in electrodermal activity measurements and the expression of stress verbatims. In parallel, a sebum production increase and a skin pH decrease were observed. A total of 198 VOCs with different potential sources were identified. They were categorized in 5 groups: probable cosmetic composition, VOCs produced by the body or its microbiota, environmental origin, and dietary intake. In our qualitative statistical approach, three VOCs were found to be correlated with stress induction and 14 compounds showed significance in the paired Wilcoxon test. Fatty-acyls derived from lipids were predominantly identified as well as ethylbenzenes. [ABSTRACT FROM AUTHOR]

The effects of air pollution on health are gaining increasing research interest with limited data on skin alterations available. It was suggested that air pollution is a trigger factor for sensitive skin (SS). However, this data was based on surveys with a lack of experimental data. SS is related to altered skin nerve endings and cutaneous neurogenic inflammation. TTe present study was to assess the in vitro effect of particulate matter (PM) on epidermis and nerve ending homeostasis. PM samples were collected according to a validated protocol. Reconstructed human epidermis (RHE, Episkin®) was exposed to PM and subsequently the supernatants were transferred to a culture of PC12 cells differentiated into sensory neurons (SN). Cell viability, axonal growth and neuropeptide‐release were measured. The modulation of the expression of different inflammatory, keratinocytes differentiation and neurites growth markers was assessed. PM samples contained a high proportion of particles with a size below 1 μm and a complex chemical composition. Transcriptomic and immunohistochemical analyses revealed that PM altered keratinocytes terminal differentiation and induced an inflammatory response. While viability and functionality of the SN were not modified, their outgrowth was significantly decreased after incubation with PM‐exposed Episkin® supernatants. This was closely related to the modification of nerve growth factor/semaphorin 3A balance. This study showed that air pollutants have negative effects on keratinocytes and sensory nerve endings including inflammatory responses. These effects are probably involved in the SS pathophysiology and might be involved in inflammatory skin disorders. [ABSTRACT FROM AUTHOR]

Sensitive skin is a clinical syndrome characterized by the occurrence of unpleasant sensations, such as pruritus, burning or pain, in response to various factors, including skincare products, water, cold, heat, or other physical and/or chemical factors. Although these symptoms suggest inflammation and the activation of peripheral innervation, the pathophysiogeny of sensitive skin remains unknown. We systematically analysed cutaneous biopsies from 50 healthy women with non-sensitive or sensitive skin and demonstrated that the intraepidermal nerve fibre density, especially that of peptidergic C-fibres, was lower in the sensitive skin group. These fibres are involved in pain, itching and temperature perception, and their degeneration may promote allodynia and similar symptoms. These results suggest that the pathophysiology of skin sensitivity resembles that of neuropathic pruritus within the context of small fibre neuropathy, and that environmental factors may alter skin innervation. [ABSTRACT FROM AUTHOR]

The article discusses the factors secreted by irradiated aged fibroblasts induce solar lentigo in pigmented reconstructed epidermis includes ultraviolet exposure, sunburn and skin diseases leading to skin cancer. It mentions the role of keratinocycte grow factor, fibroblast growth factor and stem cell factors in increasing the solar lentigo (SL), pigmentation mechanisms causing hyperpigmented macules. It also adds the importance for epidermal terminal differentiation quality.

Aging is a multifactorial process that results in progressive loss of regenerative capacity and tissue function while simultaneously favoring the development of a large array of age-related diseases. Evidence suggests that the accumulation of senescent cells in tissue promotes both normal and pathological aging. Oxic stress is a key driver of cellular senescence. Because symbiotic long-lived reef corals experience daily hyperoxic and hypoxic transitions, we hypothesized that these long-lived animals have developed specific longevity strategies in response to light. We analyzed transcriptome variation in the reef coral Stylophora pistillata during the day–night cycle and revealed a signature of the FoxO longevity pathway. We confirmed this pathway by immunofluorescence using antibodies against coral FoxO to demonstrate its nuclear translocation. Through qPCR analysis of nycthemeral variations of candidate genes under different light regimens, we found that, among genes that were specifically up- or downregulated upon exposure to light, human orthologs of two "light-up" genes (HEY1 and LONF3) exhibited anti-senescence properties in primary human fibroblasts. Therefore, these genes are interesting candidates for counteracting skin aging. We propose a large screen for other light-up genes and an investigation of the biological response of reef corals to light (e.g., metabolic switching) to elucidate these processes and identify effective interventions for promoting healthy aging in humans. [ABSTRACT FROM AUTHOR]