Regulation of claudin‐4 via p63 in human epithelial cells

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 ato...

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Veröffentlicht in:Annals of the New York Academy of Sciences 2017-10, Vol.1405 (1), p.25-31
Hauptverfasser: Kojima, Takashi, Kohno, Takayuki, Kubo, Terufumi, Kaneko, Yakuto, Kakuki, Takuya, Kakiuchi, Akito, Kurose, Makoto, Takano, Ken‐ichi, Ogasawara, Noriko, Obata, Kazufumi, Nomura, Kazuaki, Miyata, Ryo, Konno, Takumi, Ichimiya, Shingo, Himi, Tetsuo
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container_title Annals of the New York Academy of Sciences
container_volume 1405
creator Kojima, Takashi
Kohno, Takayuki
Kubo, Terufumi
Kaneko, Yakuto
Kakuki, Takuya
Kakiuchi, Akito
Kurose, Makoto
Takano, Ken‐ichi
Ogasawara, Noriko
Obata, Kazufumi
Nomura, Kazuaki
Miyata, Ryo
Konno, Takumi
Ichimiya, Shingo
Himi, Tetsuo
description 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.
doi_str_mv 10.1111/nyas.13456
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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. 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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. 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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.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28856683</pmid><doi>10.1111/nyas.13456</doi><tpages>7</tpages></addata></record>
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subjects Allergies
Atopic dermatitis
Claudin-4 - genetics
Claudin-4 - metabolism
claudin‐4
Dermatitis
Down-Regulation
Drug delivery
Drug delivery systems
Eczema
Epidermis
Epithelial cells
Epithelial Cells - metabolism
Gene expression
Humans
Keratinocytes
Keratinocytes - metabolism
nasal epithelial cells
Nasal Polyps - genetics
Nasal Polyps - metabolism
p63
Polyps
Rhinitis
Rhinitis - genetics
Rhinitis - metabolism
Ribonucleic acid
RNA
RNA-directed DNA polymerase
siRNA
Telomerase
Telomerase reverse transcriptase
Transcription Factors - genetics
Transcription Factors - metabolism
Transcriptional Activation
Tumor Suppressor Proteins - genetics
Tumor Suppressor Proteins - metabolism
Up-Regulation
title Regulation of claudin‐4 via p63 in human epithelial cells
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