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Updated: Aug 23, 2026

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates
08:19

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates

Published on: April 22, 2019

Estradiol induces proliferation of keratinocytes via a receptor mediated mechanism

S Verdier-Sevrain1, M Yaar, J Cantatore

  • 1Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118-2394, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|June 23, 2004
PubMed

Insights

Estradiol stimulates neonatal keratinocyte proliferation by binding to estrogen receptors (ER-alpha and ER-beta). This effect involves both genomic and non-genomic signaling pathways, highlighting estradiol

Area of Science:

  • Dermatology
  • Endocrinology
  • Cell Biology

Background:

  • Neonatal keratinocytes play a crucial role in skin development and barrier function.
  • Estrogen signaling is known to influence various cell types, but its specific role in neonatal keratinocytes requires further elucidation.

Purpose of the Study:

  • To investigate the effects of estradiol on neonatal keratinocyte proliferation.
  • To determine the expression of estrogen receptor (ER) isoforms in neonatal keratinocytes.
  • To elucidate the signaling mechanisms underlying estradiol-mediated keratinocyte growth.

Main Methods:

  • Binding assays to quantify estradiol interaction with keratinocytes.
  • Immunohistochemistry and Western blotting to detect ER-alpha and ER-beta expression.
  • Cell proliferation assays in the presence and absence of estradiol and anti-estrogens.
  • Analysis of intracellular signaling pathways, including extracellular signal-regulated kinases (ERK 1/2).

Main Results:

  • Estradiol binds to neonatal keratinocytes with high affinity, confirming specific estrogen binding sites.
  • Keratinocytes express both ER-alpha and ER-beta isoforms.
  • Estradiol up-regulates ER-alpha and induces keratinocyte proliferation, an effect dependent on functional estrogen receptors.
  • Estradiol-induced proliferation is mediated by both non-genomic (membrane-associated ERK 1/2 activation) and genomic (nuclear receptor activation) pathways.

Conclusions:

  • Estradiol significantly influences neonatal keratinocyte proliferation through specific estrogen receptor interactions.
  • Both genomic and non-genomic signaling pathways are involved in estradiol's proliferative effects on keratinocytes.
  • These findings suggest a role for estrogen in neonatal skin development and homeostasis.

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