elastin and Facial-Dermatoses

Chemical peeling is a common treatment in cosmetic dermatology. A peel that has been used for many years is trichloroacetic acid. Its adverse effects have for a long time been a major limitation. We present a practical review of the characteristics, mechanisms of action, indications, and complications of superficial chemical peels and of peeling with trichloroacetic acid.

Topics: Acids; Animals; Chemexfoliation; Collagen Type I; Drug Combinations; Elastin; Epidermis; Ethanol; Facial Dermatoses; Humans; Hyperpigmentation; Keratolytic Agents; Lactic Acid; Mice; Pigmentation Disorders; Precancerous Conditions; Resorcinols; Salicylates; Skin Aging; Skin Neoplasms; Trichloroacetic Acid

To delineate the molecular mechanism of transepidermal elimination of dermal elastic materials in elastosis perforans serpiginosa, the interaction between elastin and cultured keratinocytes was studied in vitro. Synthetic elastin peptide VGVAPG elicited chemotactic responses to the cultured keratinocytes at the dose of 10-9 M. Treatment of keratinocytes with 10-6 or 10-5 M elastin peptides resulted in the suppression of cell growth and the increased expression of involucrin and transglutaminase-1, markers of terminal differentiation. When cultured keratinocytes were treated with the elastin peptides, the expression of 67 kDa elastin receptor was increased. The induction of terminal differentiation by elastin peptides was attenuated by the treatment with the combination of anti-67 kDa elastin receptor antibody. The results indicate that elastin is a potent inducer of migration and terminal differentiation of cultured keratinocytes, which is mediated by the 67 kDa elastin receptor. In the lesional skins of patients with elastosis perforans serpiginosa, the 67 kDa elastin receptor was specifically expressed in the epidermis immediately surrounding the elastic materials that were being eliminated. The elastin receptor may be involved in the interaction between keratinocytes and elastin in elastosis perforans serpiginosa.

Topics: Cell Differentiation; Cell Division; Cell Movement; Chemotaxis; Connective Tissue Diseases; Elastin; Facial Dermatoses; Humans; Keratinocytes; Protein Precursors; Receptors, Cell Surface; RNA, Messenger; Transglutaminases

Degeneration of elastic tissue in acquired cutis laxa has been previously described, but microfibrils have not been adequately studied.. We determined whether the microfibrillar component of elastic tissue is affected in skin of a patient with acquired cutis laxa.. Lesional skin was examined with indirect immunofluorescence and immunoelectron microscopy with antibodies to fibrillin.. Indirect immunofluorescence showed a reduction in the distribution of fibrillin in the papillary dermis, where there was loss of the usual pattern of microfibrils perpendicular to the epidermis. Immunoelectron microscopy showed a typical distribution of elastic microfibrils around elastin of normal skin. In skin affected by cutis laxa microfibrils appeared morphologically normal but appeared less frequently in selected sites.. The microfibrillar component of elastic fibers was reduced in the papillary dermis of this patient with acquired cutis laxa.

Topics: Actin Cytoskeleton; Adult; Cutis Laxa; Elastic Tissue; Elastin; Epidermis; Facial Dermatoses; Female; Fibrillins; Fluorescent Antibody Technique; Humans; Microfilament Proteins; Microscopy, Immunoelectron