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Elastin peptides induce migration and terminal differentiation of cultured keratinocytes via 67 kDa elastin receptor in vitro: 67 kDa elastin receptor is expressed in the keratinocytes eliminating elastic materials in elastosis perforans serpiginosa.

Abstract
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.
AuthorsN Fujimoto, S Tajima, A Ishibashi
JournalThe Journal of investigative dermatology (J Invest Dermatol) Vol. 115 Issue 4 Pg. 633-9 (Oct 2000) ISSN: 0022-202X [Print] United States
PMID10998135 (Publication Type: Journal Article)
Chemical References
  • Protein Precursors
  • RNA, Messenger
  • Receptors, Cell Surface
  • elastin-binding proteins
  • involucrin
  • Elastin
  • transglutaminase NI
  • Transglutaminases
Topics
  • Cell Differentiation (drug effects)
  • Cell Division (drug effects)
  • Cell Movement (drug effects)
  • Chemotaxis (drug effects)
  • Connective Tissue Diseases (metabolism, pathology)
  • Elastin (pharmacology)
  • Facial Dermatoses
  • Humans
  • Keratinocytes (cytology, metabolism)
  • Protein Precursors (genetics)
  • RNA, Messenger (metabolism)
  • Receptors, Cell Surface (biosynthesis, physiology)
  • Transglutaminases (genetics)

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