Expression of pro‐inflammatory cytokines and mediators induced by Bisphenol A via ERK‐NFκB and JAK1/2‐STAT3 pathways in macrophages
Macrophages not only play an important role in the innate immune response but also participate in many inflammatory and infectious diseases including asthma, diabetes, obesity, cardiovascular diseases, and cancers. Bisphenol A (BPA) is the most commonly used component for plastic products. However,...
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| Veröffentlicht in: | Environmental toxicology 2019-04, Vol.34 (4), p.486-494 |
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| creator | Huang, Fu‐Mei Chang, Yu‐Chao Lee, Shiuan‐Shinn Yang, Ming‐Ling Kuan, Yu‐Hsiang |
| description | Macrophages not only play an important role in the innate immune response but also participate in many inflammatory and infectious diseases including asthma, diabetes, obesity, cardiovascular diseases, and cancers. Bisphenol A (BPA) is the most commonly used component for plastic products. However, BPA is an endocrine disruptor for mammals and participates in several inflammatory and infectious diseases. Up until now, there are no researches demonstrated the potential role of BPA in macrophage activation and its relative mechanism. BPA promoted the generation of proinflammatory cytokines IL‐1β, IL‐6, and TNFα in a concentration‐dependent manner (P |
| doi_str_mv | 10.1002/tox.22702 |
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Bisphenol A (BPA) is the most commonly used component for plastic products. However, BPA is an endocrine disruptor for mammals and participates in several inflammatory and infectious diseases. Up until now, there are no researches demonstrated the potential role of BPA in macrophage activation and its relative mechanism. BPA promoted the generation of proinflammatory cytokines IL‐1β, IL‐6, and TNFα in a concentration‐dependent manner (P < 0.05). BPA was identified to increase the expression of proinflammatory mediators NO and PGE2, and its upstream factors iNOS, COX2, and cPLA2 in a concentration‐dependent manner (P < 0.05). Phosphorylation and nuclear translocation of NF‐κB p65 were significantly induced by BPA via IκB degradation (P < 0.05). In addition, phosphorylation of ERK significantly induced by BPA at a concentration which was less than that for phosphorylation of p38 MAPK and JNK (P < 0.05). Furthermore, phosphorylation of STAT3 significantly induced by BPA at a concentration lower than that for phosphorylation of STAT1 (P < 0.05). Phosphorylation of JAK1 and JAK2 was also significantly induced by BPA in a concentration‐dependent manner (P < 0.05).]]></description><identifier>ISSN: 1520-4081</identifier><identifier>EISSN: 1522-7278</identifier><identifier>DOI: 10.1002/tox.22702</identifier><identifier>PMID: 30609183</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Asthma ; Bisphenol A ; Cardiovascular diseases ; Cell activation ; Cyclooxygenase-2 ; Cytokines ; Defence mechanisms ; Diabetes mellitus ; ERK‐NFκB ; Extracellular signal-regulated kinase ; Heart diseases ; Immune response ; Immune system ; Immunity ; Infectious diseases ; Innate immunity ; JAK1/2‐STAT3 ; Janus kinase ; Janus kinase 2 ; Macrophages ; MAP kinase ; NF-κB protein ; Nitric-oxide synthase ; Nuclear transport ; Phenols ; Phosphorylation ; proinflammatory mediators ; Prostaglandin E2 ; Stat1 protein ; Stat3 protein ; Translocation ; Tumor necrosis factor-α</subject><ispartof>Environmental toxicology, 2019-04, Vol.34 (4), p.486-494</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3532-c2e121efc6b694a3a596f1dc228bd93d350299a2f646a1a5383a83259c84fa363</citedby><cites>FETCH-LOGICAL-c3532-c2e121efc6b694a3a596f1dc228bd93d350299a2f646a1a5383a83259c84fa363</cites><orcidid>0000-0002-8991-6394</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Ftox.22702$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Ftox.22702$$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/30609183$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Fu‐Mei</creatorcontrib><creatorcontrib>Chang, Yu‐Chao</creatorcontrib><creatorcontrib>Lee, Shiuan‐Shinn</creatorcontrib><creatorcontrib>Yang, Ming‐Ling</creatorcontrib><creatorcontrib>Kuan, Yu‐Hsiang</creatorcontrib><title>Expression of pro‐inflammatory cytokines and mediators induced by Bisphenol A via ERK‐NFκB and JAK1/2‐STAT3 pathways in macrophages</title><title>Environmental toxicology</title><addtitle>Environ Toxicol</addtitle><description><![CDATA[Macrophages not only play an important role in the innate immune response but also participate in many inflammatory and infectious diseases including asthma, diabetes, obesity, cardiovascular diseases, and cancers. Bisphenol A (BPA) is the most commonly used component for plastic products. However, BPA is an endocrine disruptor for mammals and participates in several inflammatory and infectious diseases. Up until now, there are no researches demonstrated the potential role of BPA in macrophage activation and its relative mechanism. BPA promoted the generation of proinflammatory cytokines IL‐1β, IL‐6, and TNFα in a concentration‐dependent manner (P < 0.05). BPA was identified to increase the expression of proinflammatory mediators NO and PGE2, and its upstream factors iNOS, COX2, and cPLA2 in a concentration‐dependent manner (P < 0.05). Phosphorylation and nuclear translocation of NF‐κB p65 were significantly induced by BPA via IκB degradation (P < 0.05). In addition, phosphorylation of ERK significantly induced by BPA at a concentration which was less than that for phosphorylation of p38 MAPK and JNK (P < 0.05). Furthermore, phosphorylation of STAT3 significantly induced by BPA at a concentration lower than that for phosphorylation of STAT1 (P < 0.05). Phosphorylation of JAK1 and JAK2 was also significantly induced by BPA in a concentration‐dependent manner (P < 0.05).]]></description><subject>Asthma</subject><subject>Bisphenol A</subject><subject>Cardiovascular diseases</subject><subject>Cell activation</subject><subject>Cyclooxygenase-2</subject><subject>Cytokines</subject><subject>Defence mechanisms</subject><subject>Diabetes mellitus</subject><subject>ERK‐NFκB</subject><subject>Extracellular signal-regulated kinase</subject><subject>Heart diseases</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Infectious diseases</subject><subject>Innate immunity</subject><subject>JAK1/2‐STAT3</subject><subject>Janus kinase</subject><subject>Janus kinase 2</subject><subject>Macrophages</subject><subject>MAP kinase</subject><subject>NF-κB protein</subject><subject>Nitric-oxide synthase</subject><subject>Nuclear transport</subject><subject>Phenols</subject><subject>Phosphorylation</subject><subject>proinflammatory mediators</subject><subject>Prostaglandin E2</subject><subject>Stat1 protein</subject><subject>Stat3 protein</subject><subject>Translocation</subject><subject>Tumor necrosis factor-α</subject><issn>1520-4081</issn><issn>1522-7278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp1kc9O3DAQhy0E4l859AUqS1zoIaw9TrzOcUELbUFFoluJWzTrOF1DEoc4KeTWc099nj5EH4InqXeX9oDEaazR508z8yPkLWfHnDEYde7xGGDMYIPs8gQgGsNYba7eLIqZ4jtkz_tbxlgqE7lNdgSTLOVK7JKf08emNd5bV1NX0KZ1Tz9-2boosaqwc-1A9dC5O1sbT7HOaWVyu-x7auu81yan84GeWN8sTO1KOqHfLdLp9UWwfD778_tk9enT5IKPILS-zCYzQRvsFg84LBW0Qt26ZoHfjH9DtgosvTl4rvvk69l0dvohurw6_3g6uYy0SAREGgwHbgot5zKNUWCSyoLnGkDN81TkImGQpgiFjCVyTIQSqAQkqVZxgUKKfXK09oZl73vju6yyXpuyxNq43mfAZcwZqDEL6OEL9Nb1bR2mC5RSQRuOGKj3ayqs4n1riqxpbYXtkHGWLQPKQkDZKqDAvns29vNwy__kv0QCMFoDD7Y0w-umbHZ1s1b-BaMPnLs</recordid><startdate>201904</startdate><enddate>201904</enddate><creator>Huang, Fu‐Mei</creator><creator>Chang, Yu‐Chao</creator><creator>Lee, Shiuan‐Shinn</creator><creator>Yang, Ming‐Ling</creator><creator>Kuan, Yu‐Hsiang</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QH</scope><scope>7ST</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>SOI</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8991-6394</orcidid></search><sort><creationdate>201904</creationdate><title>Expression of pro‐inflammatory cytokines and mediators induced by Bisphenol A via ERK‐NFκB and JAK1/2‐STAT3 pathways in macrophages</title><author>Huang, Fu‐Mei ; Chang, Yu‐Chao ; Lee, Shiuan‐Shinn ; Yang, Ming‐Ling ; Kuan, Yu‐Hsiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3532-c2e121efc6b694a3a596f1dc228bd93d350299a2f646a1a5383a83259c84fa363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Asthma</topic><topic>Bisphenol A</topic><topic>Cardiovascular diseases</topic><topic>Cell activation</topic><topic>Cyclooxygenase-2</topic><topic>Cytokines</topic><topic>Defence mechanisms</topic><topic>Diabetes mellitus</topic><topic>ERK‐NFκB</topic><topic>Extracellular signal-regulated kinase</topic><topic>Heart diseases</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunity</topic><topic>Infectious diseases</topic><topic>Innate immunity</topic><topic>JAK1/2‐STAT3</topic><topic>Janus kinase</topic><topic>Janus kinase 2</topic><topic>Macrophages</topic><topic>MAP kinase</topic><topic>NF-κB protein</topic><topic>Nitric-oxide synthase</topic><topic>Nuclear transport</topic><topic>Phenols</topic><topic>Phosphorylation</topic><topic>proinflammatory mediators</topic><topic>Prostaglandin E2</topic><topic>Stat1 protein</topic><topic>Stat3 protein</topic><topic>Translocation</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Fu‐Mei</creatorcontrib><creatorcontrib>Chang, Yu‐Chao</creatorcontrib><creatorcontrib>Lee, Shiuan‐Shinn</creatorcontrib><creatorcontrib>Yang, Ming‐Ling</creatorcontrib><creatorcontrib>Kuan, Yu‐Hsiang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Aqualine</collection><collection>Environment Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Environmental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Fu‐Mei</au><au>Chang, Yu‐Chao</au><au>Lee, Shiuan‐Shinn</au><au>Yang, Ming‐Ling</au><au>Kuan, Yu‐Hsiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of pro‐inflammatory cytokines and mediators induced by Bisphenol A via ERK‐NFκB and JAK1/2‐STAT3 pathways in macrophages</atitle><jtitle>Environmental toxicology</jtitle><addtitle>Environ Toxicol</addtitle><date>2019-04</date><risdate>2019</risdate><volume>34</volume><issue>4</issue><spage>486</spage><epage>494</epage><pages>486-494</pages><issn>1520-4081</issn><eissn>1522-7278</eissn><abstract><![CDATA[Macrophages not only play an important role in the innate immune response but also participate in many inflammatory and infectious diseases including asthma, diabetes, obesity, cardiovascular diseases, and cancers. Bisphenol A (BPA) is the most commonly used component for plastic products. However, BPA is an endocrine disruptor for mammals and participates in several inflammatory and infectious diseases. Up until now, there are no researches demonstrated the potential role of BPA in macrophage activation and its relative mechanism. BPA promoted the generation of proinflammatory cytokines IL‐1β, IL‐6, and TNFα in a concentration‐dependent manner (P < 0.05). BPA was identified to increase the expression of proinflammatory mediators NO and PGE2, and its upstream factors iNOS, COX2, and cPLA2 in a concentration‐dependent manner (P < 0.05). Phosphorylation and nuclear translocation of NF‐κB p65 were significantly induced by BPA via IκB degradation (P < 0.05). In addition, phosphorylation of ERK significantly induced by BPA at a concentration which was less than that for phosphorylation of p38 MAPK and JNK (P < 0.05). Furthermore, phosphorylation of STAT3 significantly induced by BPA at a concentration lower than that for phosphorylation of STAT1 (P < 0.05). Phosphorylation of JAK1 and JAK2 was also significantly induced by BPA in a concentration‐dependent manner (P < 0.05).]]></abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>30609183</pmid><doi>10.1002/tox.22702</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-8991-6394</orcidid></addata></record> |
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| subjects | Asthma Bisphenol A Cardiovascular diseases Cell activation Cyclooxygenase-2 Cytokines Defence mechanisms Diabetes mellitus ERK‐NFκB Extracellular signal-regulated kinase Heart diseases Immune response Immune system Immunity Infectious diseases Innate immunity JAK1/2‐STAT3 Janus kinase Janus kinase 2 Macrophages MAP kinase NF-κB protein Nitric-oxide synthase Nuclear transport Phenols Phosphorylation proinflammatory mediators Prostaglandin E2 Stat1 protein Stat3 protein Translocation Tumor necrosis factor-α |
| title | Expression of pro‐inflammatory cytokines and mediators induced by Bisphenol A via ERK‐NFκB and JAK1/2‐STAT3 pathways in macrophages |
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