26 SKIN CARE
formation, epidermal differentiation and lipid synthesis, for a more cohesive barrier function able to lock water within the skin. HA synthesis was measured on normal
human epidermal keratinocytes (NHEK) and normal human dermal fibroblasts (NHDF), after incubation for 72 hours with our upcycled active at 0.5%. Therefore, it has been observed that HA release was respectively increased by 62% (p<0.001) and 32% (p<0.05), in treated NHEK and NHDF compared to untreated cells (control). As stated before, a major enemy of HA is
oxidative stress, influenced by various internal and external factors (UV, pollution etc.). Fortunately, skin cells can prevent free radical formation or detoxify skin tissue thanks to cell antioxidant responses. From transcriptomic analysis, ability of GSfE to act on antioxidant and oxidative stress markers has been evaluated on NHEK and NHDF treated with 1% compared to cells treated with its solvent (control). Variations of mRNA levels were expressed as percentage of control. The results highlighted an upregulation
of genes related to antioxidant defense in treated NHEK: Glutaredoxin (GLRX), Sirtuin 3 (SIRT3) and Sirtuin 7 (SIRT7) by respectively +130%, +90% and +70%. This pattern is also observable in treated NHDF: Glutaredoxin (GLRX), Glutathion S-transferase 1, Thioredoxin, Heme oxygenase 1 and Peroxiredoxin 1 (PRDX1) are upregulated by respectively +120%, +90%, +90%, +80% and +160%. In a complementary way, GSfE-incubated
NHEK showed a downregulation of Peptidylprolyl isomerase A (PPIA), an oxidative stress marker, by 40%. Therefore, more than increasing its production, GSfE also participates to HA protection. To have more information about the impact
180 160 140 120 100 80 60 40 20 0
Control CONTROL GSfE 0.5%
Hyaluronic acid
HA/CD44 conjugate
Lipid barrier formation
Keratinocyte differenciation
Tight junction formation
Figure 1: Hyaluronic acid binding to CD44 receptor signaling cascade
of HA signaling cascade, effect of GSfE on CD44 expression was observed. Immunodetection and quantification of CD44 were performed on NHEK treated with GSfE 0.5%, D-panthenol 0.3% or nothing (control). As shown in the figure below, CD44 synthesis was boosted by 42% in GSfE 0.5% treated NHEK compared to untreated ones. This induction is comparable to the one obtained with D-panthenol (reference moisturizing molecule1
). In human skin, the stratum corneum
structure prevents excessive water loss. Indeed, this cornified layer consists of terminally differentiated keratinocytes (called corneocytes) which are embedded in a lipid-containing extracellular matrix.2 These lipids, released from lamellar bodies,
are derived from de novo synthesis of lipids by keratinocytes.3
Thus, quantification of lipids
synthesis was performed by staining lipids with a lipids specific green fluorescent dye in NHEK (n=3) treated (or not, control condition) with GSfE 0.5% during 48h. Results showed that active treatment increases lipid synthesis by +147% compared to untreated keratinocytes (control). From the transcriptomic study, decorin (DCN), a specific marker of terminal NHEK differentiation,4
+42% +45%
gene expression was upregulated GSfE 0.5% D-panthenol 0.3% D-PANTHENOL 0.3%
by +840% in keratinocytes treated compared to control. Moreover, occludin (OCLN) and claudin-1 (CLDN1), tight junction makers, gene expression was also increased by respectively +90% and +70% in keratinocytes treated compared to untreated NHEK (control). As expected through the stimulation of HA signaling cascade, GSfE induces tight junction formation and skin differentiation markers, for a greater epidermal cohesion participating to skin water retention.
Figure 2: Quantification of CD44 synthesis in NHEK after treatment with GSfE 0.5% or D-panthenol 0.3%. Mean± SD, statistical significance: **p<0.01, *p<0.05 versus control
PERSONAL CARE June 2023
Water diffusion facilitation via DEJ reinforcement As dermal-epidermal junction (DEJ) is a key in water diffusion, gene expression of its specific markers was also studied. Therefore, it has been shown that fibronectin 1 (FN1), Integrin alpha-2 subunit (ITGA2) and Laminin subunit gamma 2 (LAMC2) are upregulated gene expression respectively by +110%, +60% and +80% in keratinocytes treated compared to untreated NHEK (control). Moreover, gene expression of Integrin
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Relative fluorescent unit vs control (%)
Credit: Gruber et al 2021, Vantage
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