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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]

Tissue homeostasis requires regulation of cell–cell communication, which relies on signaling molecules and cell contacts. In skin epidermis, keratinocytes secrete factors transduced by melanocytes into signaling cues promoting their pigmentation and dendrite outgrowth, while melanocytes transfer melanin pigments to keratinocytes to convey skin photoprotection. How epidermal cells integrate these functions remains poorly characterized. Here, we show that caveolae are asymmetrically distributed in melanocytes and particularly abundant at the melanocyte–keratinocyte interface in epidermis. Caveolae in melanocytes are modulated by ultraviolet radiations and keratinocytes-released factors, like miRNAs. Preventing caveolae formation in melanocytes increases melanin pigment synthesis through upregulation of cAMP signaling and decreases cell protrusions, cell–cell contacts, pigment transfer and epidermis pigmentation. Altogether, we identify that caveolae serve as molecular hubs that couple signaling outputs from keratinocytes to mechanical plasticity of pigment cells. The coordination of intercellular communication and contacts by caveolae is thus crucial to skin pigmentation and tissue homeostasis. Caveolae are plasma membrane invaginations playing crucial functions, like signal transduction and mechanoprotection. Here, the authors show that caveolae contribute to skin pigmentation by integrating the biochemical and mechanical response of epidermal melanocytes to extracellular cues. [ABSTRACT FROM AUTHOR]

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]