Dose-dependent role of claudin-1 in vivo in orchestrating features of atopic dermatitis

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  • Reitaro Tokumasu
    Laboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
  • Kosuke Yamaga
    Laboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
  • Yuji Yamazaki
    Laboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
  • Hiroyuki Murota
    Department of Dermatology, Course of integrated Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
  • Koya Suzuki
    Laboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
  • Atsushi Tamura
    Laboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
  • Kana Bando
    Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology, 2-2-3 Minatojima Minami-machi, Chuou-ku, Kobe 650-0047, Japan
  • Yasuhide Furuta
    Laboratory for Animal Resources and Genetic Engineering, RIKEN Center for Developmental Biology, 2-2-3 Minatojima Minami-machi, Chuou-ku, Kobe 650-0047, Japan
  • Ichiro Katayama
    Department of Dermatology, Course of integrated Medicine, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;
  • Sachiko Tsukita
    Laboratory of Biological Science, Graduate School of Frontier Biosciences and Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan;

Description

<jats:title>Significance</jats:title><jats:p><jats:italic>Claudin-1</jats:italic>(<jats:italic>CLDN1</jats:italic>), which is thought to be a key gene for human skin disease, especially atopic dermatitis (AD), encodes the dominant claudin responsible for the paracellular barrier at tight junctions in the epidermis. Although decreased<jats:italic>CLDN1</jats:italic>expression levels are reported in AD patients, it has been difficult to study how CLDN1 contributes to AD development, mainly because<jats:italic>Cldn1</jats:italic>knock-out mice die within 1 d after birth from dehydration. In this report, we reproduced features of human AD in mice, by systematically regulating the<jats:italic>Cldn1</jats:italic>expression level. Our experimental approach contributes to the understanding of AD’s etiology and suggests a therapeutic target for this disorder.</jats:p>

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