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Glucocorticoid-induced functional polarity of growth factor responsiveness regulates tight junction dynamics in

P Buse1, P L Woo, D B Alexander

  • 1Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA.

The Journal of Biological Chemistry
|November 24, 1995
PubMed

Insights

Dexamethasone, a glucocorticoid, promotes tight junction formation and cell polarization in mammary tumor cells. Transforming growth factor-alpha disrupts these junctions, affecting cell growth regulation.

Area of Science:

  • Cell Biology
  • Molecular Endocrinology
  • Cancer Research

Background:

  • Mammary epithelial cells exhibit specific differentiation properties, including tight junction formation.
  • Glucocorticoids like dexamethasone influence cell differentiation and growth.
  • Epidermal growth factor receptor (EGFR) signaling plays a role in cell proliferation.

Purpose of the Study:

  • To investigate the effects of dexamethasone on tight junction formation and cell polarization in Con8 mammary tumor cells.
  • To determine the role of transforming growth factor-alpha (TGF-alpha) in modulating dexamethasone-induced effects.
  • To explore the functional polarization of EGFR in response to growth factors.

Main Methods:

  • Cell culture of Con8 mammary tumor cells on permeable supports.
  • Measurement of transepithelial electrical resistance (TEER) to assess tight junction integrity.
  • Confocal immunofluorescence microscopy to visualize ZO-1 protein localization.
  • Differential administration of TGF-alpha to apical and basolateral compartments.

Main Results:

  • Dexamethasone induced "normal-like" tight junction formation and suppressed tumor cell growth.
  • Dexamethasone generated a polarized cell monolayer regarding EGFR responsiveness.
  • Basolateral TGF-alpha disrupted dexamethasone-stimulated tight junctions and caused ZO-1 redistribution.
  • TGF-alpha exerted mitogenic effects independently of tight junction disruption.

Conclusions:

  • Dexamethasone induces functional polarization of EGFR in mammary epithelial cells.
  • Glucocorticoid-regulated tight junctions are crucial for policing polarized cell responsiveness to growth factors.
  • This study provides the first evidence for functional polarization of the epidermal growth factor receptor.

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