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E-cadherin and its downstream catenins are proteolytically cleaved in human HaCaT keratinocytes exposed to UVB

Chi-Feng Hung1, Han-Sun Chiang, Huey-Ming Lo

  • 1School of Medicine, Fu-Jen Catholic University, Taipei County, Taiwan.

Experimental Dermatology
|March 4, 2006
PubMed

Insights

Ultraviolet B (UVB) irradiation causes cleavage of E-cadherin and catenins in keratinocytes undergoing apoptosis, disrupting skin barrier function and integrity.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cell Biology

Background:

  • Ultraviolet B (UVB) irradiation is known to affect melanocytes during melanoma development.
  • The impact of UVB on E-cadherin in keratinocytes remains less understood.
  • E-cadherin is crucial for cell-cell adhesion in the skin epidermis.

Purpose of the Study:

  • To investigate the effect of UVB irradiation on the E-cadherin-catenin complex in human HaCaT keratinocytes.
  • To determine the mechanisms underlying UVB-induced changes in keratinocyte cell adhesion.

Main Methods:

  • Exposure of HaCaT keratinocytes to UVB irradiation.
  • Analysis of E-cadherin and catenin protein expression and cleavage.
  • Inhibition studies using caspase and metalloproteinase inhibitors.
  • Assessment of physical association between E-cadherin and catenins.

Main Results:

  • UVB irradiation induced proteolytic cleavage of E-cadherin, beta-catenin, and gamma-catenin in apoptotic HaCaT keratinocytes.
  • Cleavage of beta- and gamma-catenin was inhibited by caspase inhibitors.
  • E-cadherin cleavage was not affected by caspase or metalloproteinase inhibitors.
  • UVB-induced cleavage disrupted the association between E-cadherin and catenins, compromising E-cadherin signaling.

Conclusions:

  • UVB irradiation compromises E-cadherin signaling in keratinocytes through proteolytic cleavage.
  • This disruption of cell-cell adhesion in keratinocytes may lead to impaired skin integrity following UVB exposure.
  • The findings highlight a novel mechanism by which UVB damages skin structure at the molecular level.

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