LONGEVISkin

What is it About?

Skin Aging is a complex phenomenon in which several mechanisms operate simultaneously. Among them, intrinsic aging is a time-dependent process, which leads to gradual skin changes affecting its structure and function. Despite much progress these last two decades in the field of skin tissue engineering, designing models of skin chronological aging remains a difficult challenge.

By using LabSkin proprietary technologies, our Skin Designers tackled this challenge by creating a unique approach for the generation of the first worldwide 3D LONGEVISkin model.

LONGEVISKIN, a “120 days” extended-time skin model

By using prolonged culture as a proxy for cellular aging, we extended to 120 days the culture time of a skin equivalent model based on our unique LabSkin matriX® scaffolding biomaterials.

Extending time in culture to 60, 75 and 120 days leads to sequential decrease of epidermal thickness accompanied by a decrease of cells expressing the proliferation marker Ki67. Epidermal thickness over time revealed a regular and significant 20% decrease in width at each time point.

Although the proliferative potential has importantly and significantly decreased, cells expressing Ki67 are still present in the basal layer, showing the maintenance of the viability of this model even after 120 days of culture.

Similar to the situation observed in vivo, the level of p16INK4A increases in the basal and the lower suprabasal layers, supporting cellular senescence process associated to our 3D LONGEVISkin model.

Epidermal differentiation profile similar to human aged skin

3D LONGEVISkin LabSkin model demonstrates the same phenotypic changes that are observed in chronological aging.

Reconstructed epidermal compartment undergoes subtle but significant structural and histological alterations similar to some aging features.

Epidermal atrophy seems to affect mostly the spinous cell layers whereas neither stratum corneum nor stratum granulosum seems to be affected. Most pronounced changes occur within the basal cells, which display an increased heterogeneity in size with an overall increased volume similar to in vivo aging process.

3D LONGEVISkin Aging model exhibits a reduction of epidermal differentiated cell layers accompanied by anomalies in the differentiation process compromising natural protective skin barrier and reflecting in vivo age-related changes.

Ultrastructural age-associated damages

Ultrastructural analysis of epidermal basement membrane showed typical features of aged skin such as duplication of lamina densa and alterations of hemidesmosomes. 

3D LONGEVISkin model exhibits irregular basement membrane, frequent reduplication of the lamina densa and disruption in hemidesmosome–keratin filament association reduction in size of the sub-basal hemidesmosome dense plates, similar to in vivo aging-related damages.

3D LONGEVISkin replicates key features of in vivo skin aging, particularly within the aged epidermis and dermis. This innovative and reliable model provides a powerful platform to simulate long-term skin aging and supports the discovery of novel molecular targets aimed at enhancing skin appearance and promoting skin longevity for dermocosmetic applications.