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Effects of B[a]P-UVA Co-Exposure on Epigenetic Marks of Isolated Skin Cells and Impact of an Arundo donax L. Extract of These Changes

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Journal of Cosmetics, Dermatological Sciences and Applications 2024年第3期14卷 253-269页

作者： Marie M. Dorr Magali Favre-Mercuret Katell Vié Richard Fitoussi Laboratoires clarins Pontoise France

Background: Extrinsic aging results from environmental stressors such as UVR or pollutants. While the effects of single pollutants are better understood, those of their combination remain poorly scrutinized. Objective: Building on a study showing downregulation of several processes upon co-exposure to B[a]P and UVA, we investigated changes induced by epigenetic marks. Materials and Methods: Human primary fibroblasts and HaCaT cells were exposed to B[a]P and UVA. After 24 hours, exposed and unexposed cells were compared to assess DNA methylation. Focusing on HaCaT, multiplex assays enabled quantifying histone H3 modifications and evaluating four splicing factors (SRSF1, SRSF3, SFPQ, and SF3B1) by immunohistochemical labeling. The expression of keratinocyte-/fibroblast-relevant genes was assessed by RT-qPCR. Finally, the impact of an Arundo donax L. extract added 24 hours before B[a]P-UVA co-exposure was analyzed. Results: Exposure to B[a]P-UVA raised DNA methylation (HaCaT: ×3.6, fibroblasts: ×1.9), an increase prevented by the extract. In HaCaT cells, B[a]P-UVA increases the frequency of S10P (+38%). When exposure was preceded by extract treatment, the frequency of several methylations was impacted. B[a]P-UVA only induced the expression of SRSF1 and SFPQ in HaCaT (+46% and +34%). Treatment with the extract abolished this effect. Co-exposure increases the expression of inflammation-related genes (IL-1α, IL-1β) in HaCaT cells and decreases those of AQP3, KRT15, and SOD2. The extract has little effect on these changes. In primary fibroblasts, exposure to B[a]P-UVA lowered the expression of LOXL2, LUM, and TGFBR2 (−38%, −59%, and −51%, respectively), and the extract did not affect these modifications. Conclusion: Within 24 hours, a single B[a]P-UVA co-exposure changes epigenetic marks of skin cells but has only mild effects on gene expression. An Arundo donax L. extract can prevent part of the epigenetic marks’ changes and could stimulate the expression of some genes in

关键词： Extrinsic Aging DNA Methylation Histone H3 Splicing Factors Arundo donax L.

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Effect of Red Panax ginsengon Mitochondrial Dynamics and Bioenergetics in HaCaT Cells Exposed to Urban Pollutants

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Journal of Cosmetics, Dermatological Sciences and Applications 2021年第2期11卷 84-95页

作者： Gallic Beauchef Magali Favre-Mercuret Beatrice Blanc Richard Fitoussi Katell Vié Nathalie Compagnone clarins research laboratory Pontoise France ICDD-sas Gemenos France Bliive Consulting Auriol France

Background: Urban air pollution contributes to lung and cardiovascular system dysfunction, making it a major concern for human health. Its impact on skin integrity, associated with increased occurrence of atopic dermatitis, is now recognized, but its cellular mechanisms remain poorly understood. Objective: In the present study we aimed at establishing the impact of urban pollutant on mitochondrial dynamics and bioenergetics using the HaCaT cell model. We also sought to establish the protective effect of ECH-5195 (red Panax ginseng extract), standardized in ginsenosides, in reversing pollution-induced mitochondrial defects. Methods: Urban pollution exposure was mimicked by 1 h exposure of HaCaT cells with standardized atmospheric particulate matter containing PAHs, nitro-PAHs, PCB congeners, and chlorinated pesticides with a mean particulate diameter of 5.85 μm (SRM1648). Results: The presence of urban pollutant in the cultures increased the prevalence of hyperfission by 1.41-fold (p = 0.023) and fission by 1.35 fold (p = 0.006) in the reticular mitochondrial network. ECH-5195 reduced both pollution-induced hyperfission by 0.54-fold (p = 0.004) and fission by 0.68-fold (p = 0.0006) normalizing the mitochondrial reticular network. Pollution exposure was associated with a significant reduction of basal OCR and increased lactate production, pushing the cell to rely on glycolysis for ATP production. When ECH-5195 was used, OCR was significantly increased, and the glycolytic contribution to ATP production was reduced while both oxidative phosphorylation and mitochondrial respiration were increased demonstrating mitochondrial re-engagement in ATP production. Conclusions: Pollution exposure was disruptive for both the mitochondrial network dynamics and mitochondrial respiration. Ginsenosides in ECH-5195 efficiently protected both from pollution-induced defects.

关键词： Ginsenosides Arylhydrocarbon Receptor Particulate Matter HaCaT Cells Mitochondria Dynamics Cell Bioenergetics

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Impact of Celosia cristataExtract on Adipogenesis of Native Human CD34+/CD31-Cells

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Journal of Cosmetics, Dermatological Sciences and Applications 2013年第3期3卷 55-63页

作者： Richard Fitoussi David Estève Anne-Sophie Delassus Katell Vié Centre de Recherche clarins Pontoise France Inserm UMR1048 Team 1 Institute of Metabolic and Cardiovascular Diseases Toulouse France

Background: The adipose tissue mainly consists of adipocytes but also contains non-adipose cells. Among them, progenitor cells represent a local pool of immature cells that, in vitro, can undergo various lineage differentiation processes. These cells are thought to contribute to normal homeostasis of the adipose tissue through adipogenesis but also to the growth of the adipose tissue under chronic energy overload. The aim of the present study is to evaluate in vitro the capacity of a Celosia cristata extract to impact the adipogenic potential of native human adipose tissue progenitor cells, i.e. commitment and differentiation towards adipogenic lineage. Methods: Native adipose tissue progenitor cells were isolated by immunoselection/depletion approaches from human subcutaneous adipose tissues. Two distinct cell culture conditions were used to assess the effect of Celosia cristata extract on commitment and differenciation of progenitor cells. Cells were cultured either in differentiation medium for 10 days in the presence/absence of Celosia cristata extracts to study the impact on differentiation or first cultured in a commitment-inducing medium, with or without Celosia cristata extract, for 48 h and then cultured 10 days in differentiation medium to assess the impact on commitment. In both experimental series, the fate of progenitor cells was studied by quantification of lipids and by determining the expression of key genes involved in adipogenesis. Results: Data show that Celosia cristata extract reduces lipid content of progenitor cells undergoing differentiation. This reduction correlates with a reduced expression of C/EBPα. When progenitor cells are placed in commitment-inducing conditions, Celosia cristata extract induces a more potent reduction of lipid content. This reduction correlates with a decrease in the expression levels of master genes involved in adipogenesis: the genes of transcription factors PPARγ2 and C/EBPα as well as marker genes coding for LPL

关键词： Adipose Tissue Stem/Progenitor Cells Adipogenic Commitment Adipogenic Differentiation

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TRPV1 and TRPA1 in cutaneous neurogenic and chronic inflammation： pro-inflammatory response induced by their activation and their sensitization

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Protein & Cell 2017年第9期8卷 644-661页

作者： Olivier Gouin Killian L'Herondelle Nicolas Lebonvallet Christelle Le Gall-lanotto Mehdi Sakka Virginie Buhe Emmanuelle PIee-Gautier Jean-Luc Carre Luc Lefeuvre Laurent Misery~,Raphaele Le Garrec laboratory on Interaction Neurons-Keratinocytes (LINK) University of Western Brittany 29200 Brest France Uriage Dermatological Laboratories 92400 Courbevoie France

Cutaneous neurogenic inflammation （CNI） is inflammation that is induced （or enhanced） in the skin by the release of neuropeptides from sensory nerve endings. Clinical manifestations are mainly sensory and vascular disorders such as pruritus and erythema. Transient receptor potential vanilloid 1 and ankyrin 1 （TRPV1 and TRPA1, respectively） are non-selective cation channels known to specifically participate in pain and CNI. Both TRPV1 and TRPA1 are co-expressed in a large subset of sensory nerves, where they integrate numerous noxious stimuli. It is now clear that the expression of both channels also extends far beyond the sensory nerves in the skin, occuring also in keratinocytes, mast cells, dendritic cells, and endothelial cells. In these non-neu- ronal cells, TRPV1 and TRPA1 also act as nociceptive sensors and potentiate the inflammatory process. This review discusses the role of TRPV1 and TRPA1 in the modulation of inflammatory genes that leads to or maintains CNI in sensory neurons and non-neuronal skin cells. In addition, this review provides a summary of current research on the intracellular sensitization pathways of both TRP channels by other endogenous inflammatory mediators that promote the self-maintenance of CNI.

关键词： sensory nervenflammation inflammatory geneneurogenic skinregulation pruritus

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