CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27
: Both CCL27 and CCL28 are ligands for CCR10 and attract CCR10+ lymphocytes. We previously demonstrated that CCL27 and CCL28 were strongly expressed in sera and lesional keratinocytes of patients with atopic dermatitis and psoriasis vulgaris. However, the regulation of CCL27 and CCL28 production in...
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| Veröffentlicht in: | Experimental dermatology 2006-02, Vol.15 (2), p.95-100 |
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| container_title | Experimental dermatology |
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| creator | Kagami, Shinji Saeki, Hidehisa Komine, Mayumi Kakinuma, Takashi Nakamura, Koichiro Tsunemi, Yuichiro Sasaki, Kiyo Asahina, Akihiko Tamaki, Kunihiko |
| description | : Both CCL27 and CCL28 are ligands for CCR10 and attract CCR10+ lymphocytes. We previously demonstrated that CCL27 and CCL28 were strongly expressed in sera and lesional keratinocytes of patients with atopic dermatitis and psoriasis vulgaris. However, the regulation of CCL27 and CCL28 production in keratinocytes has not been well documented. In this study, we showed that CCL27 and CCL28 expression and production by a human keratinocyte cell line, HaCaT cells, were strongly induced by inflammatory cytokines tumor necrosis factor‐α and interleukin‐1β. CCL27 production was downregulated by inhibitors of p38 mitogen‐activated protein kinase and nuclear factor‐kappa B (NF‐κB). By contrast, CCL28 production was downregulated by inhibitors of extracellular signal‐regulated kinase and NF‐κB. Our study results suggest that CCL28 produced by keratinocytes is mediated by different signal pathways from CCL27 and that both CCL27 and CCL28 are involved in the pathogenesis of inflammatory skin diseases. |
| doi_str_mv | 10.1111/j.1600-0625.2005.00390.x |
| format | Article |
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We previously demonstrated that CCL27 and CCL28 were strongly expressed in sera and lesional keratinocytes of patients with atopic dermatitis and psoriasis vulgaris. However, the regulation of CCL27 and CCL28 production in keratinocytes has not been well documented. In this study, we showed that CCL27 and CCL28 expression and production by a human keratinocyte cell line, HaCaT cells, were strongly induced by inflammatory cytokines tumor necrosis factor‐α and interleukin‐1β. CCL27 production was downregulated by inhibitors of p38 mitogen‐activated protein kinase and nuclear factor‐kappa B (NF‐κB). By contrast, CCL28 production was downregulated by inhibitors of extracellular signal‐regulated kinase and NF‐κB. Our study results suggest that CCL28 produced by keratinocytes is mediated by different signal pathways from CCL27 and that both CCL27 and CCL28 are involved in the pathogenesis of inflammatory skin diseases.</description><identifier>ISSN: 0906-6705</identifier><identifier>EISSN: 1600-0625</identifier><identifier>DOI: 10.1111/j.1600-0625.2005.00390.x</identifier><identifier>PMID: 16433680</identifier><language>eng</language><publisher>Oxford, UK; Malden, USA: Munksgaard International Publishers</publisher><subject>Biological and medical sciences ; Cell Line ; Chemokine CCL27 ; Chemokines - biosynthesis ; Chemokines, CC - metabolism ; Dermatitis - etiology ; Dermatitis - immunology ; Dermatitis - metabolism ; Dermatology ; epidermal growth factor receptor ; extracellular signal-regulated kinases ; Humans ; Imidazoles - pharmacology ; Interleukin-1 - pharmacology ; keratinocytes ; Keratinocytes - drug effects ; Keratinocytes - immunology ; Keratinocytes - metabolism ; Ligands ; MAP Kinase Signaling System - drug effects ; Medical sciences ; NF-kappa B - antagonists & inhibitors ; NF-kappa B - metabolism ; nuclear factor-kappa B ; p38 mitogen-activated protein kinases ; Pyridines - pharmacology ; Receptors, CCR10 ; Receptors, Chemokine - metabolism ; Sesquiterpenes - pharmacology ; Signal Transduction - drug effects ; Tumor Necrosis Factor-alpha - pharmacology</subject><ispartof>Experimental dermatology, 2006-02, Vol.15 (2), p.95-100</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5000-ebc2bf2ec7c4ad92b99f265fcf730efbafe21d405d351b19a36e17a948905f7f3</citedby><cites>FETCH-LOGICAL-c5000-ebc2bf2ec7c4ad92b99f265fcf730efbafe21d405d351b19a36e17a948905f7f3</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%2Fj.1600-0625.2005.00390.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1600-0625.2005.00390.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17575972$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16433680$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kagami, Shinji</creatorcontrib><creatorcontrib>Saeki, Hidehisa</creatorcontrib><creatorcontrib>Komine, Mayumi</creatorcontrib><creatorcontrib>Kakinuma, Takashi</creatorcontrib><creatorcontrib>Nakamura, Koichiro</creatorcontrib><creatorcontrib>Tsunemi, Yuichiro</creatorcontrib><creatorcontrib>Sasaki, Kiyo</creatorcontrib><creatorcontrib>Asahina, Akihiko</creatorcontrib><creatorcontrib>Tamaki, Kunihiko</creatorcontrib><title>CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27</title><title>Experimental dermatology</title><addtitle>Exp Dermatol</addtitle><description>: Both CCL27 and CCL28 are ligands for CCR10 and attract CCR10+ lymphocytes. We previously demonstrated that CCL27 and CCL28 were strongly expressed in sera and lesional keratinocytes of patients with atopic dermatitis and psoriasis vulgaris. However, the regulation of CCL27 and CCL28 production in keratinocytes has not been well documented. In this study, we showed that CCL27 and CCL28 expression and production by a human keratinocyte cell line, HaCaT cells, were strongly induced by inflammatory cytokines tumor necrosis factor‐α and interleukin‐1β. CCL27 production was downregulated by inhibitors of p38 mitogen‐activated protein kinase and nuclear factor‐kappa B (NF‐κB). By contrast, CCL28 production was downregulated by inhibitors of extracellular signal‐regulated kinase and NF‐κB. Our study results suggest that CCL28 produced by keratinocytes is mediated by different signal pathways from CCL27 and that both CCL27 and CCL28 are involved in the pathogenesis of inflammatory skin diseases.</description><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Chemokine CCL27</subject><subject>Chemokines - biosynthesis</subject><subject>Chemokines, CC - metabolism</subject><subject>Dermatitis - etiology</subject><subject>Dermatitis - immunology</subject><subject>Dermatitis - metabolism</subject><subject>Dermatology</subject><subject>epidermal growth factor receptor</subject><subject>extracellular signal-regulated kinases</subject><subject>Humans</subject><subject>Imidazoles - pharmacology</subject><subject>Interleukin-1 - pharmacology</subject><subject>keratinocytes</subject><subject>Keratinocytes - drug effects</subject><subject>Keratinocytes - immunology</subject><subject>Keratinocytes - metabolism</subject><subject>Ligands</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Medical sciences</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-kappa B - metabolism</subject><subject>nuclear factor-kappa B</subject><subject>p38 mitogen-activated protein kinases</subject><subject>Pyridines - pharmacology</subject><subject>Receptors, CCR10</subject><subject>Receptors, Chemokine - metabolism</subject><subject>Sesquiterpenes - pharmacology</subject><subject>Signal Transduction - drug effects</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><issn>0906-6705</issn><issn>1600-0625</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUGPEyEYhonRuLX6FwwXvc34MRQoiRcd112TRg_WrPFCvmFAqdOZCtO0_fcyttm9ygUSnvfjzQMhlEHJ8nqzKZkEKEBWoqwARAnANZTHR2R2f_GYzECDLKQCcUWepbQBYIor8ZRcMbngXC5hRtZ1vaqWdBeHdm_HMPQ09PQWa1xT67ou0QMmunVtwNG1tDnRNnjvoutHmsLPHju6w_HXAU-J-jhs6TROPSdPPHbJvbjsc_Lt4_W6vi1WX24-1e9WhRWQW7rGVo2vnFV2ga2uGq19JYW3XnFwvkHvKtYuQLRcsIZp5NIxhXqx1CC88nxOXp_n5vp_9i6NZhvSVBt7N-yTUaAqzpnO4PIM2jikFJ03uxi2GE-GgZmMmo2ZxJlJnJmMmn9GzTFHX17e2DfZw0PwojADry4AJoudj9jbkB44JZTQucecvD1zh9C5038XMNffP-RDjhfneEijO97HMf42cvpVc_f5xvyA9-IrX0lzx_8CxEKfAA</recordid><startdate>200602</startdate><enddate>200602</enddate><creator>Kagami, Shinji</creator><creator>Saeki, Hidehisa</creator><creator>Komine, Mayumi</creator><creator>Kakinuma, Takashi</creator><creator>Nakamura, Koichiro</creator><creator>Tsunemi, Yuichiro</creator><creator>Sasaki, Kiyo</creator><creator>Asahina, Akihiko</creator><creator>Tamaki, Kunihiko</creator><general>Munksgaard International Publishers</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>200602</creationdate><title>CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27</title><author>Kagami, Shinji ; Saeki, Hidehisa ; Komine, Mayumi ; Kakinuma, Takashi ; Nakamura, Koichiro ; Tsunemi, Yuichiro ; Sasaki, Kiyo ; Asahina, Akihiko ; Tamaki, Kunihiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5000-ebc2bf2ec7c4ad92b99f265fcf730efbafe21d405d351b19a36e17a948905f7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Chemokine CCL27</topic><topic>Chemokines - biosynthesis</topic><topic>Chemokines, CC - metabolism</topic><topic>Dermatitis - etiology</topic><topic>Dermatitis - immunology</topic><topic>Dermatitis - metabolism</topic><topic>Dermatology</topic><topic>epidermal growth factor receptor</topic><topic>extracellular signal-regulated kinases</topic><topic>Humans</topic><topic>Imidazoles - pharmacology</topic><topic>Interleukin-1 - pharmacology</topic><topic>keratinocytes</topic><topic>Keratinocytes - drug effects</topic><topic>Keratinocytes - immunology</topic><topic>Keratinocytes - metabolism</topic><topic>Ligands</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Medical sciences</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>NF-kappa B - metabolism</topic><topic>nuclear factor-kappa B</topic><topic>p38 mitogen-activated protein kinases</topic><topic>Pyridines - pharmacology</topic><topic>Receptors, CCR10</topic><topic>Receptors, Chemokine - metabolism</topic><topic>Sesquiterpenes - pharmacology</topic><topic>Signal Transduction - drug effects</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kagami, Shinji</creatorcontrib><creatorcontrib>Saeki, Hidehisa</creatorcontrib><creatorcontrib>Komine, Mayumi</creatorcontrib><creatorcontrib>Kakinuma, Takashi</creatorcontrib><creatorcontrib>Nakamura, Koichiro</creatorcontrib><creatorcontrib>Tsunemi, Yuichiro</creatorcontrib><creatorcontrib>Sasaki, Kiyo</creatorcontrib><creatorcontrib>Asahina, Akihiko</creatorcontrib><creatorcontrib>Tamaki, Kunihiko</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kagami, Shinji</au><au>Saeki, Hidehisa</au><au>Komine, Mayumi</au><au>Kakinuma, Takashi</au><au>Nakamura, Koichiro</au><au>Tsunemi, Yuichiro</au><au>Sasaki, Kiyo</au><au>Asahina, Akihiko</au><au>Tamaki, Kunihiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27</atitle><jtitle>Experimental dermatology</jtitle><addtitle>Exp Dermatol</addtitle><date>2006-02</date><risdate>2006</risdate><volume>15</volume><issue>2</issue><spage>95</spage><epage>100</epage><pages>95-100</pages><issn>0906-6705</issn><eissn>1600-0625</eissn><abstract>: Both CCL27 and CCL28 are ligands for CCR10 and attract CCR10+ lymphocytes. We previously demonstrated that CCL27 and CCL28 were strongly expressed in sera and lesional keratinocytes of patients with atopic dermatitis and psoriasis vulgaris. However, the regulation of CCL27 and CCL28 production in keratinocytes has not been well documented. In this study, we showed that CCL27 and CCL28 expression and production by a human keratinocyte cell line, HaCaT cells, were strongly induced by inflammatory cytokines tumor necrosis factor‐α and interleukin‐1β. CCL27 production was downregulated by inhibitors of p38 mitogen‐activated protein kinase and nuclear factor‐kappa B (NF‐κB). By contrast, CCL28 production was downregulated by inhibitors of extracellular signal‐regulated kinase and NF‐κB. Our study results suggest that CCL28 produced by keratinocytes is mediated by different signal pathways from CCL27 and that both CCL27 and CCL28 are involved in the pathogenesis of inflammatory skin diseases.</abstract><cop>Oxford, UK; Malden, USA</cop><pub>Munksgaard International Publishers</pub><pmid>16433680</pmid><doi>10.1111/j.1600-0625.2005.00390.x</doi><tpages>6</tpages></addata></record> |
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| ispartof | Experimental dermatology, 2006-02, Vol.15 (2), p.95-100 |
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| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Biological and medical sciences Cell Line Chemokine CCL27 Chemokines - biosynthesis Chemokines, CC - metabolism Dermatitis - etiology Dermatitis - immunology Dermatitis - metabolism Dermatology epidermal growth factor receptor extracellular signal-regulated kinases Humans Imidazoles - pharmacology Interleukin-1 - pharmacology keratinocytes Keratinocytes - drug effects Keratinocytes - immunology Keratinocytes - metabolism Ligands MAP Kinase Signaling System - drug effects Medical sciences NF-kappa B - antagonists & inhibitors NF-kappa B - metabolism nuclear factor-kappa B p38 mitogen-activated protein kinases Pyridines - pharmacology Receptors, CCR10 Receptors, Chemokine - metabolism Sesquiterpenes - pharmacology Signal Transduction - drug effects Tumor Necrosis Factor-alpha - pharmacology |
| title | CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27 |
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