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Importance of transient receptor potential vanilloid 4 (TRPV4) in epidermal barrier function in human skin keratinocytes
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  • 作者:Naoko Kida (1) (2)
    Takaaki Sokabe (2)
    Makiko Kashio (2)
    Kunitaka Haruna (3)
    Yuki Mizuno (3)
    Yasushi Suga (3)
    Kazuko Nishikawa (1)
    Akiko Kanamaru (1)
    Maya Hongo (1)
    Ai Oba (1)
    Makoto Tominaga (2) (4)
  • 关键词:Transient receptor potential vanilloid 4 ; Epidermal barrier ; Temperature ; Tight junction
  • 刊名:Pfl眉gers Archiv - European Journal of Physiology
  • 出版年:2012
  • 出版时间:May 2012
  • 年:2012
  • 卷:463
  • 期:5
  • 页码:715-725
  • 全文大小:615KB
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  • 作者单位:Naoko Kida (1) (2)
    Takaaki Sokabe (2)
    Makiko Kashio (2)
    Kunitaka Haruna (3)
    Yuki Mizuno (3)
    Yasushi Suga (3)
    Kazuko Nishikawa (1)
    Akiko Kanamaru (1)
    Maya Hongo (1)
    Ai Oba (1)
    Makoto Tominaga (2) (4)

    1. POLA Chemical Industries, Inc., Yokohama, Japan
    2. Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), National Institutes of Natural Sciences, Okazaki, Japan
    3. Department of Dermatology, Juntendo University Urayasu Hospital, Urayasu, Japan
    4. Department of Physiological Sciences, The Graduate University for Advanced Studies, Okazaki, Japan
  • ISSN:1432-2013
文摘
The state of the skin changes drastically depending on the ambient temperature. Skin epidermal keratinocytes express thermosensitive transient receptor potential vanilloid (TRPV) cation channels, TRPV3 and TRPV4. These multimodal receptors are activated by various kinds of chemical and physical stimuli, including warm temperatures (>30°C). It has been suggested that TRPV4 is involved in cell–cell junction maturation; however, the effect of temperature fluctuations on TRPV4-dependent barrier homeostasis is unclear. In the present study, we demonstrated that activation of TRPV4 was crucial for barrier formation and recovery, both of which were critical for the prevention of excess dehydration of human skin keratinocytes. TRPV4 activation by physiological skin temperature (33°C), GSK1016790A or 4α-PDD allowed influx of Ca2+ from extracellular spaces which promoted cell–cell junction development. These changes resulted in augmentation of intercellular barrier integrity in vitro and ex vivo. TRPV4 disruption reduced the increase in trans-epidermal resistance and increased intercellular permeation after a Ca2+ switch. Furthermore, barrier recovery after the disruption of the stratum corneum was accelerated by the activation of TRPV4 either by warm temperature or a chemical activator. Our results suggest that physiological skin temperatures play important roles in cell–cell junction and skin barrier homeostasis through TRPV4 activation.

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