4‐phenylpyridine suppresses UVB‐induced skin inflammation by targeting c‐Src in vitro and in vivo
Acute or repetitive exposure to ultraviolet (UV) cause disruptions to the skin barrier and subsequent inflammatory skin disease. 4‐phenylpyridine (4‐PP) is a constituent of Brassica campestris L. ssp. Pekinensis and its effect on skin inflammation and molecular target remain unclear. The purpose of...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2022-07, Vol.26 (14), p.3891-3901 |
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| creator | Kim, Ju Gyeong Kang, Ha Yeong Kim, Min Jeong Lim, Seokwon Lee, Chang Joo Kim, Kyung‐Min Jung, Sung Keun |
| description | Acute or repetitive exposure to ultraviolet (UV) cause disruptions to the skin barrier and subsequent inflammatory skin disease. 4‐phenylpyridine (4‐PP) is a constituent of Brassica campestris L. ssp. Pekinensis and its effect on skin inflammation and molecular target remain unclear. The purpose of this study is to confirm the anti‐inflammatory efficacy of 4‐PP on UVB‐induced skin inflammation in human keratinocytes HaCaT and mouse skin and validation of its molecular target. 4‐PP also attenuated UVB‐induced phosphorylation of p38/mitogen‐activated protein kinase kinase (MKK) 3/6, c‐Jun N‐terminal kinase 1/2, MKK 4/7, extracellular‐signal‐regulated kinase 1/2, mitogen‐activated protein kinase 1/2. Additionally, 4‐PP inhibited UVB‐induced phosphorylation of epidermal growth factor receptor (EGFR) Y1068, Y1045 and 854 residues but not the proto‐oncogene tyrosine‐protein kinase c‐Src. Drug affinity responsive target stability assay revealed that 4‐PP directly binds to c‐Src and inhibits pronase c‐proteolysis. Knockdown of c‐Src inhibited UVB‐induced COX‐2 expression and phosphorylation of MAPKs and EGFR in HaCaT cells. Dorsal treatment of 4‐PP prevented UVB (0.5 J/cm2)‐induced skin thickness, phosphorylation of EGFR and COX‐2 expression in mouse skin. Our findings suggest that 4‐PP can be used as anti‐inflammatory agent with an effect of skin inflammation by inhibiting the COX‐2 expression via suppressing the c‐Src/EGFR/MAPKs signalling pathway. |
| doi_str_mv | 10.1111/jcmm.17422 |
| format | Article |
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Pekinensis and its effect on skin inflammation and molecular target remain unclear. The purpose of this study is to confirm the anti‐inflammatory efficacy of 4‐PP on UVB‐induced skin inflammation in human keratinocytes HaCaT and mouse skin and validation of its molecular target. 4‐PP also attenuated UVB‐induced phosphorylation of p38/mitogen‐activated protein kinase kinase (MKK) 3/6, c‐Jun N‐terminal kinase 1/2, MKK 4/7, extracellular‐signal‐regulated kinase 1/2, mitogen‐activated protein kinase 1/2. Additionally, 4‐PP inhibited UVB‐induced phosphorylation of epidermal growth factor receptor (EGFR) Y1068, Y1045 and 854 residues but not the proto‐oncogene tyrosine‐protein kinase c‐Src. Drug affinity responsive target stability assay revealed that 4‐PP directly binds to c‐Src and inhibits pronase c‐proteolysis. Knockdown of c‐Src inhibited UVB‐induced COX‐2 expression and phosphorylation of MAPKs and EGFR in HaCaT cells. Dorsal treatment of 4‐PP prevented UVB (0.5 J/cm2)‐induced skin thickness, phosphorylation of EGFR and COX‐2 expression in mouse skin. Our findings suggest that 4‐PP can be used as anti‐inflammatory agent with an effect of skin inflammation by inhibiting the COX‐2 expression via suppressing the c‐Src/EGFR/MAPKs signalling pathway.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.17422</identifier><identifier>PMID: 35686492</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>4‐phenylpyridine ; Animals ; Biotechnology ; Brassica campestris L. ssp. pekinensis ; COX‐2 ; c‐Src ; Enzymes ; Epidermal growth factor ; Epidermal growth factor receptors ; Gene expression ; Inflammation ; JNK protein ; Keratinocytes ; Kinases ; Original ; Pathogens ; Phosphorylation ; phytochemicals ; Pronase ; Protein kinase C ; Proteins ; Proteolysis ; Signal transduction ; Skin cancer ; Skin diseases ; skin inflammation ; Src protein ; Tyrosine ; Ultraviolet radiation</subject><ispartof>Journal of cellular and molecular medicine, 2022-07, Vol.26 (14), p.3891-3901</ispartof><rights>2022 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4482-b040f3cb561f6347de5096d129951fea75b302f885594531a829c5dd55ff2bb83</citedby><cites>FETCH-LOGICAL-c4482-b040f3cb561f6347de5096d129951fea75b302f885594531a829c5dd55ff2bb83</cites><orcidid>0000-0002-0956-7367</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279582/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279582/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35686492$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Ju Gyeong</creatorcontrib><creatorcontrib>Kang, Ha Yeong</creatorcontrib><creatorcontrib>Kim, Min Jeong</creatorcontrib><creatorcontrib>Lim, Seokwon</creatorcontrib><creatorcontrib>Lee, Chang Joo</creatorcontrib><creatorcontrib>Kim, Kyung‐Min</creatorcontrib><creatorcontrib>Jung, Sung Keun</creatorcontrib><title>4‐phenylpyridine suppresses UVB‐induced skin inflammation by targeting c‐Src in vitro and in vivo</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Acute or repetitive exposure to ultraviolet (UV) cause disruptions to the skin barrier and subsequent inflammatory skin disease. 4‐phenylpyridine (4‐PP) is a constituent of Brassica campestris L. ssp. Pekinensis and its effect on skin inflammation and molecular target remain unclear. The purpose of this study is to confirm the anti‐inflammatory efficacy of 4‐PP on UVB‐induced skin inflammation in human keratinocytes HaCaT and mouse skin and validation of its molecular target. 4‐PP also attenuated UVB‐induced phosphorylation of p38/mitogen‐activated protein kinase kinase (MKK) 3/6, c‐Jun N‐terminal kinase 1/2, MKK 4/7, extracellular‐signal‐regulated kinase 1/2, mitogen‐activated protein kinase 1/2. Additionally, 4‐PP inhibited UVB‐induced phosphorylation of epidermal growth factor receptor (EGFR) Y1068, Y1045 and 854 residues but not the proto‐oncogene tyrosine‐protein kinase c‐Src. Drug affinity responsive target stability assay revealed that 4‐PP directly binds to c‐Src and inhibits pronase c‐proteolysis. Knockdown of c‐Src inhibited UVB‐induced COX‐2 expression and phosphorylation of MAPKs and EGFR in HaCaT cells. Dorsal treatment of 4‐PP prevented UVB (0.5 J/cm2)‐induced skin thickness, phosphorylation of EGFR and COX‐2 expression in mouse skin. Our findings suggest that 4‐PP can be used as anti‐inflammatory agent with an effect of skin inflammation by inhibiting the COX‐2 expression via suppressing the c‐Src/EGFR/MAPKs signalling pathway.</description><subject>4‐phenylpyridine</subject><subject>Animals</subject><subject>Biotechnology</subject><subject>Brassica campestris L. ssp. pekinensis</subject><subject>COX‐2</subject><subject>c‐Src</subject><subject>Enzymes</subject><subject>Epidermal growth factor</subject><subject>Epidermal growth factor receptors</subject><subject>Gene expression</subject><subject>Inflammation</subject><subject>JNK protein</subject><subject>Keratinocytes</subject><subject>Kinases</subject><subject>Original</subject><subject>Pathogens</subject><subject>Phosphorylation</subject><subject>phytochemicals</subject><subject>Pronase</subject><subject>Protein kinase C</subject><subject>Proteins</subject><subject>Proteolysis</subject><subject>Signal transduction</subject><subject>Skin cancer</subject><subject>Skin diseases</subject><subject>skin inflammation</subject><subject>Src protein</subject><subject>Tyrosine</subject><subject>Ultraviolet radiation</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kctu1DAUhiMEoqWw4QGQJTao0hRfE3uDBKNyUysWULaW48vUQ2KndjIoOx6BZ-RJ8JChAhZ4c2ydT__5ff6qeozgGSrn-Vb3_RlqKMZ3qmPEOF5RQejdwx1xwo-qBzlvISQ1IuJ-dURYzWsq8HG1oT--fR-ubZi7YU7e-GBBnoYh2ZxtBlefX5W-D2bS1oD8xQfgg-tU36vRxwDaGYwqbezowwbogn5MuhBg58cUgQpmeeziw-qeU122jw71pLp6ff5p_XZ18eHNu_XLi5WmtJhtIYWO6JbVyNWENsYyKGqDsBAMOasa1hKIHeeMCcoIUhwLzYxhzDnctpycVC8W3WFqe2u0DWNSnRyS71WaZVRe_t0J_lpu4k4K3IiyriLw7CCQ4s1k8yh7n7XtOhVsnLLEdcNqSCnaz3r6D7qNUwrle4XivGkKxgp1ulA6xZyTdbdmEJT7_OQ-P_krvwI_-dP-Lfo7sAKgBfjqOzv_R0q-X19eLqI_AafrqYM</recordid><startdate>202207</startdate><enddate>202207</enddate><creator>Kim, Ju 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suppresses UVB‐induced skin inflammation by targeting c‐Src in vitro and in vivo</title><author>Kim, Ju Gyeong ; Kang, Ha Yeong ; Kim, Min Jeong ; Lim, Seokwon ; Lee, Chang Joo ; Kim, Kyung‐Min ; Jung, Sung Keun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4482-b040f3cb561f6347de5096d129951fea75b302f885594531a829c5dd55ff2bb83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>4‐phenylpyridine</topic><topic>Animals</topic><topic>Biotechnology</topic><topic>Brassica campestris L. ssp. pekinensis</topic><topic>COX‐2</topic><topic>c‐Src</topic><topic>Enzymes</topic><topic>Epidermal growth factor</topic><topic>Epidermal growth factor receptors</topic><topic>Gene expression</topic><topic>Inflammation</topic><topic>JNK protein</topic><topic>Keratinocytes</topic><topic>Kinases</topic><topic>Original</topic><topic>Pathogens</topic><topic>Phosphorylation</topic><topic>phytochemicals</topic><topic>Pronase</topic><topic>Protein kinase C</topic><topic>Proteins</topic><topic>Proteolysis</topic><topic>Signal transduction</topic><topic>Skin cancer</topic><topic>Skin diseases</topic><topic>skin inflammation</topic><topic>Src protein</topic><topic>Tyrosine</topic><topic>Ultraviolet radiation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Ju Gyeong</creatorcontrib><creatorcontrib>Kang, Ha Yeong</creatorcontrib><creatorcontrib>Kim, Min Jeong</creatorcontrib><creatorcontrib>Lim, Seokwon</creatorcontrib><creatorcontrib>Lee, Chang Joo</creatorcontrib><creatorcontrib>Kim, Kyung‐Min</creatorcontrib><creatorcontrib>Jung, Sung Keun</creatorcontrib><collection>Wiley Online Library Open 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vitro and in vivo</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2022-07</date><risdate>2022</risdate><volume>26</volume><issue>14</issue><spage>3891</spage><epage>3901</epage><pages>3891-3901</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Acute or repetitive exposure to ultraviolet (UV) cause disruptions to the skin barrier and subsequent inflammatory skin disease. 4‐phenylpyridine (4‐PP) is a constituent of Brassica campestris L. ssp. Pekinensis and its effect on skin inflammation and molecular target remain unclear. The purpose of this study is to confirm the anti‐inflammatory efficacy of 4‐PP on UVB‐induced skin inflammation in human keratinocytes HaCaT and mouse skin and validation of its molecular target. 4‐PP also attenuated UVB‐induced phosphorylation of p38/mitogen‐activated protein kinase kinase (MKK) 3/6, c‐Jun N‐terminal kinase 1/2, MKK 4/7, extracellular‐signal‐regulated kinase 1/2, mitogen‐activated protein kinase 1/2. Additionally, 4‐PP inhibited UVB‐induced phosphorylation of epidermal growth factor receptor (EGFR) Y1068, Y1045 and 854 residues but not the proto‐oncogene tyrosine‐protein kinase c‐Src. Drug affinity responsive target stability assay revealed that 4‐PP directly binds to c‐Src and inhibits pronase c‐proteolysis. Knockdown of c‐Src inhibited UVB‐induced COX‐2 expression and phosphorylation of MAPKs and EGFR in HaCaT cells. Dorsal treatment of 4‐PP prevented UVB (0.5 J/cm2)‐induced skin thickness, phosphorylation of EGFR and COX‐2 expression in mouse skin. Our findings suggest that 4‐PP can be used as anti‐inflammatory agent with an effect of skin inflammation by inhibiting the COX‐2 expression via suppressing the c‐Src/EGFR/MAPKs signalling pathway.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>35686492</pmid><doi>10.1111/jcmm.17422</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-0956-7367</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 4‐phenylpyridine Animals Biotechnology Brassica campestris L. ssp. pekinensis COX‐2 c‐Src Enzymes Epidermal growth factor Epidermal growth factor receptors Gene expression Inflammation JNK protein Keratinocytes Kinases Original Pathogens Phosphorylation phytochemicals Pronase Protein kinase C Proteins Proteolysis Signal transduction Skin cancer Skin diseases skin inflammation Src protein Tyrosine Ultraviolet radiation |
| title | 4‐phenylpyridine suppresses UVB‐induced skin inflammation by targeting c‐Src in vitro and in vivo |
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