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Regulation of claudin‐4 via p63 in human epithelial cells
Author(s) -
Kojima Takashi,
Kohno Takayuki,
Kubo Terufumi,
Kaneko Yakuto,
Kakuki Takuya,
Kakiuchi Akito,
Kurose Makoto,
Takano Kenichi,
Ogasawara Noriko,
Obata Kazufumi,
Nomura Kazuaki,
Miyata Ryo,
Konno Takumi,
Ichimiya Shingo,
Himi Tetsuo
Publication year - 2017
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.13456
Subject(s) - downregulation and upregulation , claudin , transfection , gene knockdown , small interfering rna , microbiology and biotechnology , epidermis (zoology) , tight junction , telomerase reverse transcriptase , epithelium , regulator , human skin , cell culture , gene silencing , biology , immunology , chemistry , telomerase , gene , anatomy , genetics
P63 is a regulator of cell–cell junction complexes in the epidermis. Claudin‐4 is regulated via various factors in normal epithelial cells and diseases. We found that claudin‐4 was directly regulated via p63 (TAp63 and ΔNp63) in human keratinocytes and nasal epithelial cells. In the epidermis of atopic dermatitis (AD), which contains ΔNp63‐deficient keratinocytes, high expression of claudin‐4 was observed. In primary keratinocytes, downregulation of ΔNp63 by treatment with short interfering RNA (siRNA)‐p63 induced claudin‐4 expression. In nasal epithelial cells in the context of rhinitis or nasal polyps, upregulation of TAp63 and downregulation of claudin‐4 were observed. In primary nasal epithelial cells transfected with the human telomerase reverse transcriptase gene, knockdown of p63 by siRNAs induced claudin‐4 expression. Taken together, these findings indicate that p63 is a negative regulator of claudin‐4 expression. Understanding the regulation of claudin‐4 via p63 in human epithelial cells may be important for developing therapies for allergies and drug delivery systems.