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Eicosapentanoic acid increases aquaporin‐3 expression in human skin keratinocytes (647.49)
Author(s) -
Mun YeunJa,
Jeon ByoungKook,
Woo WonHong,
Lee YoungEun
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.647.49
Subject(s) - hacat , aquaporin 3 , aquaporin , epidermis (zoology) , chemistry , microbiology and biotechnology , keratinocyte , arachidonic acid , human skin , polyunsaturated fatty acid , biochemistry , fatty acid , biology , in vitro , enzyme , anatomy , genetics
Eicosapentanoic acid (EPA), an omega‐3 polyunsaturated fatty acids (ω‐3 PUFAs), protects against photodamage and photocarcinogenesis in mammals. Water movement across the plasma membrane can occur via two pathways: by diffusion through the lipid bilayer and by membrane inserted water channels (aquaporins; AQPs). At least 13 subtypes, denoted AQP0‐AQP12, have so far been identified in mammalian cells. AQP3 is a water/glycerol transporting protein in basal layer keratinocytes of epidermis in normal skin. We have investigated the effects of EPA on AQP3 expression and the effects of EPA on ultraviolet (UV)‐induced AQP3 down˗regulation in cultured human skin keratinocytes. EPA treatment increased AQP3 gene and protein expression in human epidermal keratinocytes (HaCaT). Using a specific inhibitor, we observed that the effect of EPA on AQP3 expression was mediated by ERK activation. UV induced AQP3 down‐regulation in HaCaT cells. EPA treatment attenuated UV‐induced AQP3 loss and cell death. Collectively, the present results show that EPA increased AQP3 expression and protected against photodamage of UV through the induction of AQP3 expression.