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E‐cadherin and its downstream catenins are proteolytically cleaved in human HaCaT keratinocytes exposed to UVB
Author(s) -
Hung ChiFeng,
Chiang HanSun,
Lo HueyMing,
Jian JrShian,
Wu WenBin
Publication year - 2006
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.0906-6705.2006.00411.x
Subject(s) - hacat , cadherin , keratinocyte , catenin , cleavage (geology) , microbiology and biotechnology , apoptosis , beta catenin , chemistry , biology , signal transduction , cell , in vitro , biochemistry , wnt signaling pathway , paleontology , fracture (geology)
It has been reported that ultraviolet B (UVB) irradiation causes the loss of E‐cadherin of melanocytes, leading them to escape from neighboring keratinocytes during melanoma development. However, little has been paid on its effect on E‐cadherin of keratinocytes. In the present study we therefore focus on whether UVB affects expression of E‐cadherin‐catenin complex in human HaCaT keratinocytes. We found that E‐cadherin, β‐, and γ‐catenin but not α‐catenin were proteolytically cleaved in UVB‐irradiated HaCaT keratinocytes. The effect was only observed in keratinocyte undergoing apoptosis. Cleavage of β‐ and γ‐catenin was fully abolished by caspase‐3 and caspase‐8 inhibitors, whereas cleavage of E‐cadherin was inhibited by neither caspase nor metalloproteinase inhibitors. Functional analysis showed that the cleavage resulted in the disruption of the physical association between E‐cadherin and catenins, indicating that E‐cadherin signaling was compromised in UVB‐irradiated HaCaT keratinocytes. Because E‐cadherin in keratinocytes plays important roles in mediating cell–cell adhesion in epidermis of skin, the loss of E‐cadherin and signaling components in keratinocytes may lead to the disruption of skin integrity after UVB exposure.