Lack of desquamation - the Achilles heel of the reconstructed epidermis.

The use of human skin equivalents for screening tests aiming to assess repetitive application of various test agents is hampered by the lack of desquamation in vitro. The present study was undertaken to examine whether the desquamation can be induced by various treatments including mechanical stress, application of various agents that should decrease the surface pH and calcium level, activate the enzymes involved in desquamation process or UV irradiation. In addition, the effect of alpha-hydroxyacids, known to enhance desquamation and to improve the stratum corneum barrier function in vivo, was examined as well.

Water distribution and natural moisturizer factor content in human skin equivalents are regulated by environmental relative humidity.

Human skin equivalents (HSEs) show great similarities to human native skin. However, one of the key processes impaired under in vitro conditions is desquamation. Desquamation involves the degradation of the corneodesmosomes, in which various enzymes participate.

Endothelial network formed with human dermal microvascular endothelial cells in autologous multicellular skin substitutes.

A human skin equivalent from a single skin biopsy harboring keratinocytes and melanocytes in the epidermal compartment, and fibroblasts and microvascular dermal endothelial cells in the dermal compartment was developed. The results of the study revealed that the nature of the extracellular matrix of the dermal compartments plays an important role in establishment of endothelial network in vitro. With rat-tail type I collagen matrices only lateral but not vertical expansion of endothelial networks was observed.

Proteomic profiling identifies an UV-induced activation of cofilin-1 and destrin in human epidermis.

The human skin is the only line of defense against UV radiation. A series of responses to protect the skin are induced by UV radiation. In this study, a proteomic approach was used to study these responses.

Human adipose tissue-derived cells delay re-epithelialization in comparison with skin fibroblasts in organotypic skin culture.

Background: Wound healing of deep and extensive burns can induce hypertrophic scar formation. During the early steps of wound healing fibroblasts migrate into the wounded area. Fibroblastic cells present in tissues other than dermis may also migrate into the wounded area and participate in the wound healing process.