Effect of S100A8 and S100A9 on expressions of cytokine and skin barrier protein in human keratinocytes
Atopic dermatitis (AD) is an inflammatory skin disorder caused by immunological dysregulation and genetic factors. Whether the expression levels of cytokine and skin barrier protein were altered by S100 calcium binding protein A8 (S100A8) and S100A9 in human keratinocytic HaCaT cells was examined in...
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| Veröffentlicht in: | Molecular medicine reports 2019-09, Vol.20 (3), p.2476-2483 |
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| creator | Kim, Mun Jeong Im, Mi Ae Lee, Ji-Sook Mun, Ji Young Kim, Da Hye Gu, Ayoung Kim, In Sik |
| description | Atopic dermatitis (AD) is an inflammatory skin disorder caused by immunological dysregulation and genetic factors. Whether the expression levels of cytokine and skin barrier protein were altered by S100 calcium binding protein A8 (S100A8) and S100A9 in human keratinocytic HaCaT cells was examined in the present study. Alterations of cytokine expression were examined by ELISA following treatment with S100A8/9 and various signal protein‑specific inhibitors. Activation of the mitogen activated protein kinase (MAPK) pathway and nuclear factor (NF)‑κB was evaluated by using western blotting and an NF‑κB activity test, respectively. The expression levels of interleukin (IL)‑6, IL‑8 and monocyte chemoattractant protein‑1 increased following treatment with S100A8 and S100A9, and the increase was significantly blocked by specific signaling pathway inhibitors, including toll‑like receptor 4 inhibitor (TLR4i), rottlerin, PD98059, SB203580 and BAY‑11‑7085. Extracellular signal‑regulated kinase (ERK) and p38 MAPK pathways were activated in a time‑dependent manner following treatment with S100A8 and S100A9. Phosphorylation of ERK and p38 MAPK were blocked by TLR4i and rottlerin. S100A8 and S100A9 induced translocation of NF‑κB in a time‑dependent manner, and the activation of NF‑κB was inhibited by TLR4i, rottlerin, PD98059 and SB203580. In addition, S100A8 and S100A9 decreased the expression of skin barrier proteins, filaggrin and loricrin. These results may help to elucidate the pathogenic mechanisms of AD and develop clinical strategies for controlling AD. |
| doi_str_mv | 10.3892/mmr.2019.10454 |
| format | Article |
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Whether the expression levels of cytokine and skin barrier protein were altered by S100 calcium binding protein A8 (S100A8) and S100A9 in human keratinocytic HaCaT cells was examined in the present study. Alterations of cytokine expression were examined by ELISA following treatment with S100A8/9 and various signal protein‑specific inhibitors. Activation of the mitogen activated protein kinase (MAPK) pathway and nuclear factor (NF)‑κB was evaluated by using western blotting and an NF‑κB activity test, respectively. The expression levels of interleukin (IL)‑6, IL‑8 and monocyte chemoattractant protein‑1 increased following treatment with S100A8 and S100A9, and the increase was significantly blocked by specific signaling pathway inhibitors, including toll‑like receptor 4 inhibitor (TLR4i), rottlerin, PD98059, SB203580 and BAY‑11‑7085. Extracellular signal‑regulated kinase (ERK) and p38 MAPK pathways were activated in a time‑dependent manner following treatment with S100A8 and S100A9. Phosphorylation of ERK and p38 MAPK were blocked by TLR4i and rottlerin. S100A8 and S100A9 induced translocation of NF‑κB in a time‑dependent manner, and the activation of NF‑κB was inhibited by TLR4i, rottlerin, PD98059 and SB203580. In addition, S100A8 and S100A9 decreased the expression of skin barrier proteins, filaggrin and loricrin. These results may help to elucidate the pathogenic mechanisms of AD and develop clinical strategies for controlling AD.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2019.10454</identifier><identifier>PMID: 31322196</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Apoptosis ; Atopic dermatitis ; Calcium-binding protein ; Calgranulin A - immunology ; Calgranulin B - immunology ; Cell Line ; Chemokines ; Cytokines ; Cytokines - analysis ; Cytokines - immunology ; Defects ; Dermatitis ; Dermatitis, Atopic - immunology ; Eczema ; Enzyme-linked immunosorbent assay ; Extracellular signal-regulated kinase ; Filaggrin ; Genetic factors ; Humans ; Immunoglobulins ; Interleukin 8 ; Keratinocytes ; Keratinocytes - immunology ; Kinases ; MAP kinase ; MAP Kinase Signaling System ; Membrane Proteins - analysis ; Membrane Proteins - immunology ; Monocyte chemoattractant protein ; Monocyte chemoattractant protein 1 ; Monocytes ; NF-kappa B - analysis ; NF-kappa B - immunology ; NF-κB protein ; Pathogenesis ; Phosphorylation ; Protein kinase ; Proteins ; Rheumatoid arthritis ; S100 Proteins - analysis ; S100 Proteins - immunology ; Signal transduction ; TLR4 protein ; Toll-like receptors ; Transcription factors ; Tumor necrosis factor-TNF ; Western blotting</subject><ispartof>Molecular medicine reports, 2019-09, Vol.20 (3), p.2476-2483</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c363t-5bf52ccf9be13c4153b8a7a2bb79851b5db5b4c700d7e0fc8474c51cb9de48d63</citedby><cites>FETCH-LOGICAL-c363t-5bf52ccf9be13c4153b8a7a2bb79851b5db5b4c700d7e0fc8474c51cb9de48d63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31322196$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Mun Jeong</creatorcontrib><creatorcontrib>Im, Mi Ae</creatorcontrib><creatorcontrib>Lee, Ji-Sook</creatorcontrib><creatorcontrib>Mun, Ji Young</creatorcontrib><creatorcontrib>Kim, Da Hye</creatorcontrib><creatorcontrib>Gu, Ayoung</creatorcontrib><creatorcontrib>Kim, In Sik</creatorcontrib><title>Effect of S100A8 and S100A9 on expressions of cytokine and skin barrier protein in human keratinocytes</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Atopic dermatitis (AD) is an inflammatory skin disorder caused by immunological dysregulation and genetic factors. Whether the expression levels of cytokine and skin barrier protein were altered by S100 calcium binding protein A8 (S100A8) and S100A9 in human keratinocytic HaCaT cells was examined in the present study. Alterations of cytokine expression were examined by ELISA following treatment with S100A8/9 and various signal protein‑specific inhibitors. Activation of the mitogen activated protein kinase (MAPK) pathway and nuclear factor (NF)‑κB was evaluated by using western blotting and an NF‑κB activity test, respectively. The expression levels of interleukin (IL)‑6, IL‑8 and monocyte chemoattractant protein‑1 increased following treatment with S100A8 and S100A9, and the increase was significantly blocked by specific signaling pathway inhibitors, including toll‑like receptor 4 inhibitor (TLR4i), rottlerin, PD98059, SB203580 and BAY‑11‑7085. Extracellular signal‑regulated kinase (ERK) and p38 MAPK pathways were activated in a time‑dependent manner following treatment with S100A8 and S100A9. Phosphorylation of ERK and p38 MAPK were blocked by TLR4i and rottlerin. S100A8 and S100A9 induced translocation of NF‑κB in a time‑dependent manner, and the activation of NF‑κB was inhibited by TLR4i, rottlerin, PD98059 and SB203580. In addition, S100A8 and S100A9 decreased the expression of skin barrier proteins, filaggrin and loricrin. These results may help to elucidate the pathogenic mechanisms of AD and develop clinical strategies for controlling AD.</description><subject>Apoptosis</subject><subject>Atopic dermatitis</subject><subject>Calcium-binding protein</subject><subject>Calgranulin A - immunology</subject><subject>Calgranulin B - immunology</subject><subject>Cell Line</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Cytokines - analysis</subject><subject>Cytokines - immunology</subject><subject>Defects</subject><subject>Dermatitis</subject><subject>Dermatitis, Atopic - immunology</subject><subject>Eczema</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Extracellular signal-regulated kinase</subject><subject>Filaggrin</subject><subject>Genetic factors</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Interleukin 8</subject><subject>Keratinocytes</subject><subject>Keratinocytes - immunology</subject><subject>Kinases</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System</subject><subject>Membrane Proteins - analysis</subject><subject>Membrane Proteins - immunology</subject><subject>Monocyte chemoattractant protein</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>NF-kappa B - analysis</subject><subject>NF-kappa B - immunology</subject><subject>NF-κB protein</subject><subject>Pathogenesis</subject><subject>Phosphorylation</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Rheumatoid arthritis</subject><subject>S100 Proteins - analysis</subject><subject>S100 Proteins - immunology</subject><subject>Signal transduction</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>Transcription factors</subject><subject>Tumor necrosis factor-TNF</subject><subject>Western blotting</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkc1LAzEQxYMoVqtXj7LgxUtrPjebYyn1Awoe1POSZCe4bXdTk12w_73ZtnoQBuYN_OYxzEPohuApKxR9aJowpZioKcFc8BN0QaQiE4YxPz1qqpQcocsYVxjnggp1jkaMMEqJyi-QWzgHtsu8y94IxrMi0211kCrzbQbf2wAx1r6NA2N3nV_XLeypmFRmdAg1hGwbfAdpTvXZN7rN1hB0V7c-rUC8QmdObyJcH_sYfTwu3ufPk-Xr08t8tpxYlrNuIowT1FqnDBBmORHMFFpqaoxUhSBGVEYYbiXGlQTsbMElt4JYoyrgRZWzMbo_-KZzvnqIXdnU0cJmo1vwfSwpzQmVXAiS0Lt_6Mr3oU3XJUqyXIhCDobTA2WDjzGAK7ehbnTYlQSXQwJlSqAcEij3CaSF26Ntbxqo_vDfl7MfeUaAag</recordid><startdate>20190901</startdate><enddate>20190901</enddate><creator>Kim, Mun Jeong</creator><creator>Im, Mi Ae</creator><creator>Lee, Ji-Sook</creator><creator>Mun, Ji Young</creator><creator>Kim, Da Hye</creator><creator>Gu, Ayoung</creator><creator>Kim, In Sik</creator><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20190901</creationdate><title>Effect of S100A8 and S100A9 on expressions of cytokine and skin barrier protein in human keratinocytes</title><author>Kim, Mun Jeong ; Im, Mi Ae ; Lee, Ji-Sook ; Mun, Ji Young ; Kim, Da Hye ; Gu, Ayoung ; Kim, In Sik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c363t-5bf52ccf9be13c4153b8a7a2bb79851b5db5b4c700d7e0fc8474c51cb9de48d63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Apoptosis</topic><topic>Atopic dermatitis</topic><topic>Calcium-binding protein</topic><topic>Calgranulin A - immunology</topic><topic>Calgranulin B - immunology</topic><topic>Cell Line</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Cytokines - analysis</topic><topic>Cytokines - immunology</topic><topic>Defects</topic><topic>Dermatitis</topic><topic>Dermatitis, Atopic - immunology</topic><topic>Eczema</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Extracellular signal-regulated kinase</topic><topic>Filaggrin</topic><topic>Genetic factors</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Interleukin 8</topic><topic>Keratinocytes</topic><topic>Keratinocytes - immunology</topic><topic>Kinases</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System</topic><topic>Membrane Proteins - analysis</topic><topic>Membrane Proteins - immunology</topic><topic>Monocyte chemoattractant protein</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>NF-kappa B - analysis</topic><topic>NF-kappa B - immunology</topic><topic>NF-κB protein</topic><topic>Pathogenesis</topic><topic>Phosphorylation</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>Rheumatoid arthritis</topic><topic>S100 Proteins - analysis</topic><topic>S100 Proteins - immunology</topic><topic>Signal transduction</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><topic>Transcription factors</topic><topic>Tumor necrosis factor-TNF</topic><topic>Western blotting</topic><toplevel>online_resources</toplevel><creatorcontrib>Kim, Mun Jeong</creatorcontrib><creatorcontrib>Im, Mi Ae</creatorcontrib><creatorcontrib>Lee, Ji-Sook</creatorcontrib><creatorcontrib>Mun, Ji Young</creatorcontrib><creatorcontrib>Kim, Da Hye</creatorcontrib><creatorcontrib>Gu, Ayoung</creatorcontrib><creatorcontrib>Kim, In Sik</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Mun Jeong</au><au>Im, Mi Ae</au><au>Lee, Ji-Sook</au><au>Mun, Ji Young</au><au>Kim, Da Hye</au><au>Gu, Ayoung</au><au>Kim, In Sik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of S100A8 and S100A9 on expressions of cytokine and skin barrier protein in human keratinocytes</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2019-09-01</date><risdate>2019</risdate><volume>20</volume><issue>3</issue><spage>2476</spage><epage>2483</epage><pages>2476-2483</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Atopic dermatitis (AD) is an inflammatory skin disorder caused by immunological dysregulation and genetic factors. Whether the expression levels of cytokine and skin barrier protein were altered by S100 calcium binding protein A8 (S100A8) and S100A9 in human keratinocytic HaCaT cells was examined in the present study. Alterations of cytokine expression were examined by ELISA following treatment with S100A8/9 and various signal protein‑specific inhibitors. Activation of the mitogen activated protein kinase (MAPK) pathway and nuclear factor (NF)‑κB was evaluated by using western blotting and an NF‑κB activity test, respectively. The expression levels of interleukin (IL)‑6, IL‑8 and monocyte chemoattractant protein‑1 increased following treatment with S100A8 and S100A9, and the increase was significantly blocked by specific signaling pathway inhibitors, including toll‑like receptor 4 inhibitor (TLR4i), rottlerin, PD98059, SB203580 and BAY‑11‑7085. Extracellular signal‑regulated kinase (ERK) and p38 MAPK pathways were activated in a time‑dependent manner following treatment with S100A8 and S100A9. Phosphorylation of ERK and p38 MAPK were blocked by TLR4i and rottlerin. S100A8 and S100A9 induced translocation of NF‑κB in a time‑dependent manner, and the activation of NF‑κB was inhibited by TLR4i, rottlerin, PD98059 and SB203580. In addition, S100A8 and S100A9 decreased the expression of skin barrier proteins, filaggrin and loricrin. These results may help to elucidate the pathogenic mechanisms of AD and develop clinical strategies for controlling AD.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>31322196</pmid><doi>10.3892/mmr.2019.10454</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Atopic dermatitis Calcium-binding protein Calgranulin A - immunology Calgranulin B - immunology Cell Line Chemokines Cytokines Cytokines - analysis Cytokines - immunology Defects Dermatitis Dermatitis, Atopic - immunology Eczema Enzyme-linked immunosorbent assay Extracellular signal-regulated kinase Filaggrin Genetic factors Humans Immunoglobulins Interleukin 8 Keratinocytes Keratinocytes - immunology Kinases MAP kinase MAP Kinase Signaling System Membrane Proteins - analysis Membrane Proteins - immunology Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Monocytes NF-kappa B - analysis NF-kappa B - immunology NF-κB protein Pathogenesis Phosphorylation Protein kinase Proteins Rheumatoid arthritis S100 Proteins - analysis S100 Proteins - immunology Signal transduction TLR4 protein Toll-like receptors Transcription factors Tumor necrosis factor-TNF Western blotting |
| title | Effect of S100A8 and S100A9 on expressions of cytokine and skin barrier protein in human keratinocytes |
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