Lotti Roberta, Cattuzzato Laetitia, Huang Xuefeng, Garandeau David, Palazzo Elisabetta, Quadri Marika, Delluc Cécile, Magdeleine Eddy, Li Xiaojing, Frechet Mathilde, Marconi Alessandra
DermoLAB, Surgical, Medical, Dental and Morphological Sciences Department, University of Modena and Reggio Emilia, 41124 Modena, Italy.
Research and Development Department, Lucas Meyer Cosmetics, Clariant, 31036 Toulouse, France.
Cells. 2025 Jul 30;14(15):1176. doi: 10.3390/cells14151176.
Skin aging is characterized by compromised epidermal homeostasis and dermo-epidermal junction (DEJ) integrity, resulting in reduced stem cell potential and impaired tissue regeneration. This study investigated the effects of extract (APE) on keratinocyte stem cells (KSCs) and DEJ composition in human skin. Using human skin explants and cell culture models, we demonstrated that APE treatment enhances DEJ composition by increasing Collagen IV and Laminin production while decreasing MMP-9 expression, without altering epidermal structure or differentiation. In the same model, APE preserved stemness potential by upregulating markers related to niche components (collagen XVII and β1-integrin), proliferation (Ki-67 and KRT15), and stem cell capacity (Survivin and LRIG1). In vitro studies revealed that APE selectively stimulated KSC proliferation without affecting transit amplifying cells and promoted Collagen IV and Laminin secretion, particularly in KSCs. Furthermore, in a co-culture model simulating a compromised DEJ (UVB-induced), APE increased Laminin production in KSCs, suggesting a protective effect against photo-damage. These findings indicate that APE enhances DEJ composition and preserves stem cell potential, highlighting its promise as a candidate for skin anti-aging strategies targeting stem cell maintenance and extracellular matrix stability to promote skin regeneration and repair.
皮肤老化的特征是表皮稳态受损和真皮-表皮连接(DEJ)完整性受损,导致干细胞潜能降低和组织再生受损。本研究调查了提取物(APE)对人皮肤角质形成干细胞(KSCs)和DEJ组成的影响。使用人皮肤外植体和细胞培养模型,我们证明APE处理通过增加IV型胶原蛋白和层粘连蛋白的产生,同时降低MMP-9表达来增强DEJ组成,而不改变表皮结构或分化。在同一模型中,APE通过上调与微环境成分(XVII型胶原蛋白和β1整合素)、增殖(Ki-67和KRT15)以及干细胞能力(生存素和LRIG1)相关的标志物来保留干性潜能。体外研究表明,APE选择性地刺激KSC增殖而不影响过渡扩增细胞,并促进IV型胶原蛋白和层粘连蛋白的分泌,尤其是在KSCs中。此外,在模拟受损DEJ(紫外线诱导)的共培养模型中,APE增加了KSCs中层粘连蛋白的产生,表明其对光损伤有保护作用。这些发现表明,APE增强了DEJ组成并保留了干细胞潜能,突出了其作为皮肤抗老化策略候选物的前景,该策略旨在通过维持干细胞和细胞外基质稳定性来促进皮肤再生和修复。