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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Cultivating a Three-dimensional Reconstructed Human Epidermis at a Large Scale
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Barrier function regulates epidermal DNA synthesis.

E Proksch1, K R Feingold, M Q Man

  • 1Dermatology Service, Veterans Administration Medical Center, San Francisco, California 94121.

The Journal of Clinical Investigation
|May 1, 1991
PubMed
Summary
This summary is machine-generated.

The skin barrier regulates epidermal DNA synthesis. Disrupting the skin barrier increases DNA synthesis, while restoring it normalizes these levels, indicating a direct regulatory role.

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Area of Science:

  • Dermatology
  • Skin Biology
  • Epidermal Homeostasis

Background:

  • The skin's permeability barrier is crucial for maintaining homeostasis.
  • The relationship between barrier function and epidermal cell proliferation is not fully understood.

Purpose of the Study:

  • To investigate whether the cutaneous permeability barrier regulates epidermal DNA synthesis.
  • To explore the link between barrier disruption and increased DNA synthesis in various models.

Main Methods:

  • Utilized four models of barrier perturbation: acetone treatment, tape stripping, essential fatty acid deficiency, and chronic topical lovastatin.
  • Employed artificial membranes to occlude the skin and assessed DNA synthesis.
  • Administered topical lipids to restore barrier function.
  • Conducted autoradiographic studies to pinpoint the location of increased DNA synthesis.

Main Results:

  • All tested models showed significant increases in epidermal DNA synthesis following barrier disruption (102% with acetone, 127% with tape stripping, 50% with EFA deficiency, 64% with lovastatin).
  • Artificial barrier replacement inhibited DNA synthesis increases, with inhibition directly proportional to membrane impermeability.
  • Lipid treatment that restored barrier function normalized DNA synthesis.
  • Acetone-induced DNA synthesis increase was confined to the epidermal basal layer and did not affect protein synthesis.

Conclusions:

  • Cutaneous barrier function is a key regulator of epidermal DNA synthesis.
  • Barrier disruption triggers a specific increase in basal cell DNA synthesis.
  • These findings differentiate barrier regulation from general injury responses.