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.