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 |
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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. Understanding the regulation of claudin‐4 via p63 in human epithelial cells may be important for developing therapies for allergies and drug delivery systems.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1111/nyas.13456</identifier><identifier>PMID: 28856683</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>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</subject><ispartof>Annals of the New York Academy of Sciences, 2017-10, Vol.1405 (1), p.25-31</ispartof><rights>2017 New York Academy of Sciences.</rights><rights>2017 The New York Academy of Sciences</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4236-66da055df8fc3528dd7dce29c6005dcbea49f307adab68383dd099d6aeeb4b1f3</citedby><cites>FETCH-LOGICAL-c4236-66da055df8fc3528dd7dce29c6005dcbea49f307adab68383dd099d6aeeb4b1f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fnyas.13456$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fnyas.13456$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28856683$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kojima, Takashi</creatorcontrib><creatorcontrib>Kohno, Takayuki</creatorcontrib><creatorcontrib>Kubo, Terufumi</creatorcontrib><creatorcontrib>Kaneko, Yakuto</creatorcontrib><creatorcontrib>Kakuki, Takuya</creatorcontrib><creatorcontrib>Kakiuchi, Akito</creatorcontrib><creatorcontrib>Kurose, Makoto</creatorcontrib><creatorcontrib>Takano, Ken‐ichi</creatorcontrib><creatorcontrib>Ogasawara, Noriko</creatorcontrib><creatorcontrib>Obata, Kazufumi</creatorcontrib><creatorcontrib>Nomura, Kazuaki</creatorcontrib><creatorcontrib>Miyata, Ryo</creatorcontrib><creatorcontrib>Konno, Takumi</creatorcontrib><creatorcontrib>Ichimiya, Shingo</creatorcontrib><creatorcontrib>Himi, Tetsuo</creatorcontrib><title>Regulation of claudin‐4 via p63 in human epithelial cells</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann N Y Acad Sci</addtitle><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.</description><subject>Allergies</subject><subject>Atopic dermatitis</subject><subject>Claudin-4 - genetics</subject><subject>Claudin-4 - metabolism</subject><subject>claudin‐4</subject><subject>Dermatitis</subject><subject>Down-Regulation</subject><subject>Drug delivery</subject><subject>Drug delivery systems</subject><subject>Eczema</subject><subject>Epidermis</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - metabolism</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Keratinocytes</subject><subject>Keratinocytes - metabolism</subject><subject>nasal epithelial cells</subject><subject>Nasal Polyps - genetics</subject><subject>Nasal Polyps - metabolism</subject><subject>p63</subject><subject>Polyps</subject><subject>Rhinitis</subject><subject>Rhinitis - genetics</subject><subject>Rhinitis - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA-directed DNA polymerase</subject><subject>siRNA</subject><subject>Telomerase</subject><subject>Telomerase reverse transcriptase</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Transcriptional Activation</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Up-Regulation</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90MtKAzEYBeAgiq3VjQ8gA25EmJrbZBJcleINioKXhashk2RsJHNx0lG68xF8Rp_E1KkuXPhv_s3H4XAA2EdwjMKdVEvpx4jQhG2AIUqpiBkjeBMMIUzTmAtMBmDH-2cIEeY03QYDzHnCGCdDcHprnjonF7auorqIlJOdttXn-weNXq2MGkYiW0XzrpRVZBq7mBtnpYuUcc7vgq1COm_21n8EHs7P7qeX8ezm4mo6mcWKYsJCGS1hkuiCF4okmGudamWwUAzCRKvcSCoKAlOpZR46caI1FEIzaUxOc1SQETjqc5u2fumMX2Sl9asGsjJ15zMkCMUcQygCPfxDn-uurUK7oGiaEEx5EtRxr1Rbe9-aImtaW8p2mSGYrSbNVpNm35MGfLCO7PLS6F_6s2EAqAdv1pnlP1HZ9ePkrg_9Ao8ZgQI</recordid><startdate>201710</startdate><enddate>201710</enddate><creator>Kojima, Takashi</creator><creator>Kohno, Takayuki</creator><creator>Kubo, Terufumi</creator><creator>Kaneko, Yakuto</creator><creator>Kakuki, Takuya</creator><creator>Kakiuchi, Akito</creator><creator>Kurose, Makoto</creator><creator>Takano, Ken‐ichi</creator><creator>Ogasawara, Noriko</creator><creator>Obata, Kazufumi</creator><creator>Nomura, Kazuaki</creator><creator>Miyata, Ryo</creator><creator>Konno, Takumi</creator><creator>Ichimiya, Shingo</creator><creator>Himi, Tetsuo</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7ST</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>SOI</scope><scope>7X8</scope></search><sort><creationdate>201710</creationdate><title>Regulation of claudin‐4 via p63 in human epithelial cells</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4236-66da055df8fc3528dd7dce29c6005dcbea49f307adab68383dd099d6aeeb4b1f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Allergies</topic><topic>Atopic dermatitis</topic><topic>Claudin-4 - genetics</topic><topic>Claudin-4 - metabolism</topic><topic>claudin‐4</topic><topic>Dermatitis</topic><topic>Down-Regulation</topic><topic>Drug delivery</topic><topic>Drug delivery systems</topic><topic>Eczema</topic><topic>Epidermis</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - metabolism</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Keratinocytes</topic><topic>Keratinocytes - metabolism</topic><topic>nasal epithelial cells</topic><topic>Nasal Polyps - genetics</topic><topic>Nasal Polyps - metabolism</topic><topic>p63</topic><topic>Polyps</topic><topic>Rhinitis</topic><topic>Rhinitis - genetics</topic><topic>Rhinitis - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA-directed DNA polymerase</topic><topic>siRNA</topic><topic>Telomerase</topic><topic>Telomerase reverse transcriptase</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Transcriptional Activation</topic><topic>Tumor Suppressor Proteins - 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Academic</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kojima, Takashi</au><au>Kohno, Takayuki</au><au>Kubo, Terufumi</au><au>Kaneko, Yakuto</au><au>Kakuki, Takuya</au><au>Kakiuchi, Akito</au><au>Kurose, Makoto</au><au>Takano, Ken‐ichi</au><au>Ogasawara, Noriko</au><au>Obata, Kazufumi</au><au>Nomura, Kazuaki</au><au>Miyata, Ryo</au><au>Konno, Takumi</au><au>Ichimiya, Shingo</au><au>Himi, Tetsuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of claudin‐4 via p63 in human epithelial cells</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann N Y Acad Sci</addtitle><date>2017-10</date><risdate>2017</risdate><volume>1405</volume><issue>1</issue><spage>25</spage><epage>31</epage><pages>25-31</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><abstract>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.</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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