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Epidermal growth in the skin equivalent.

J Fransson1, H Hammar

  • 1Department of Dermatology, Karolinska Sjukhuset, Stockholm, Sweden.

Archives of Dermatological Research
|January 1, 1992
PubMed
Summary
This summary is machine-generated.

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Skin equivalents (SEs) model keratinocyte proliferation, showing initial migration then increased cell division by day 21. This model mimics findings in psoriasis and wound healing, validating its use for studying these skin conditions.

Area of Science:

  • Tissue engineering
  • Dermatology
  • Cell biology

Background:

  • Skin equivalents (SEs) are validated models for studying keratinocyte proliferation.
  • SEs are constructed using fibroblasts within a collagen matrix, seeded with skin biopsies.
  • Previous studies have established SEs for research applications.

Purpose of the Study:

  • To validate skin equivalents (SEs) as a model for keratinocyte proliferation.
  • To investigate proliferation markers in SEs during different culture stages.
  • To compare SE proliferation with psoriatic skin characteristics.

Main Methods:

  • Constructed SEs from normal skin biopsies on dermal equivalents.
  • Measured outgrowth using planimetry.
  • Performed immunohistochemistry on SEs (SE6, SE21) and psoriatic skin using Ki-67, cytokeratin 8.12, epidermal growth factor receptor (EGFr), and transferrin receptor (TFr) antibodies.

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Main Results:

  • SE area increased linearly for 7 days, attributed to keratinocyte migration.
  • By day 21 (SE21), SEs showed proliferation markers (Ki-67, cytokeratin 8.12) and receptor expression (EGFr, TFr) similar to psoriatic lesions.
  • Psoriatic lesions exhibited increased expression of EGFr and TFr in basal and suprabasal layers.

Conclusions:

  • Initial SE growth is via migration; significant proliferation occurs by day 21.
  • SEs accurately model keratinocyte proliferation seen in psoriasis and wound healing.
  • SEs are suitable models for investigating skin proliferation phenomena.