Green Tea Polyphenol EGCG Upregulates Tollip Expression by Suppressing Elf-1 Expression
TLR signaling is critical to innate immune system regulation; however, aberrant TLR signaling is involved in several diseases, including insulin resistance, Alzheimer's disease, and tumor metastasis. Moreover, a recent study found that TLR-4 signaling pathway inhibition might be a target for th...
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| Veröffentlicht in: | The Journal of immunology (1950) 2017-11, Vol.199 (9), p.3261-3269 |
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| container_title | The Journal of immunology (1950) |
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| creator | Kumazoe, Motofumi Yamashita, Mai Nakamura, Yuki Takamatsu, Kanako Bae, Jaehoon Yamashita, Shuya Yamada, Shuhei Onda, Hiroaki Nojiri, Takashi Kangawa, Kenji Tachibana, Hirofumi |
| description | TLR signaling is critical to innate immune system regulation; however, aberrant TLR signaling is involved in several diseases, including insulin resistance, Alzheimer's disease, and tumor metastasis. Moreover, a recent study found that TLR-4 signaling pathway inhibition might be a target for the suppression of chronic inflammatory disorders. In this article, we show that the green tea polyphenol epigallocatechin-3-
-gallate (EGCG) increases the expression of Toll interacting protein, a strong inhibitor of TLR4 signaling, by suppressing the expression of E74-like ETS transcription factor 1 (Elf-1). A mechanistic study revealed that EGCG suppressed Elf-1 expression via protein phosphatase 2A/cyclic GMP (cGMP)-dependent mechanisms. We also confirmed that orally administered EGCG and a cGMP inducer upregulated Toll interacting protein expression, increased intracellular levels of cGMP in macrophages, and suppressed Elf-1 expression. These data support EGCG and a cGMP inducer as potential candidate suppressors of TLR4 signaling. |
| doi_str_mv | 10.4049/jimmunol.1601822 |
| format | Article |
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-gallate (EGCG) increases the expression of Toll interacting protein, a strong inhibitor of TLR4 signaling, by suppressing the expression of E74-like ETS transcription factor 1 (Elf-1). A mechanistic study revealed that EGCG suppressed Elf-1 expression via protein phosphatase 2A/cyclic GMP (cGMP)-dependent mechanisms. We also confirmed that orally administered EGCG and a cGMP inducer upregulated Toll interacting protein expression, increased intracellular levels of cGMP in macrophages, and suppressed Elf-1 expression. These data support EGCG and a cGMP inducer as potential candidate suppressors of TLR4 signaling.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1601822</identifier><identifier>PMID: 28954885</identifier><language>eng</language><publisher>United States: American Association of Immunologists</publisher><subject>Animals ; Catechin - analogs & derivatives ; Catechin - chemistry ; Catechin - pharmacology ; Cyclic GMP ; Cyclic GMP - genetics ; Cyclic GMP - immunology ; Disease resistance ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - immunology ; Epigallocatechin gallate ; ETS protein ; Green tea ; Immune system ; Inflammatory diseases ; Innate immunity ; Insulin ; Intracellular levels ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - immunology ; Macrophages ; Male ; Metastases ; Mice ; Mice, Inbred BALB C ; Nuclear Proteins - genetics ; Nuclear Proteins - immunology ; Oral administration ; Phosphoprotein phosphatase ; Protein phosphatase ; Protein Phosphatase 2 - genetics ; Protein Phosphatase 2 - immunology ; Proteins ; Second Messenger Systems - genetics ; Second Messenger Systems - immunology ; Signal transduction ; Tea ; Tea - chemistry ; TLR4 protein ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - immunology ; Toll-like receptors ; Transcription Factors - genetics ; Transcription Factors - immunology ; Up-Regulation - immunology</subject><ispartof>The Journal of immunology (1950), 2017-11, Vol.199 (9), p.3261-3269</ispartof><rights>Copyright © 2017 by The American Association of Immunologists, Inc.</rights><rights>Copyright American Association of Immunologists Nov 1, 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-e9f2f9aec9ed7704ce043706d3deaf9b88de3f2100d12181046bc3183dd74eff3</citedby><cites>FETCH-LOGICAL-c435t-e9f2f9aec9ed7704ce043706d3deaf9b88de3f2100d12181046bc3183dd74eff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28954885$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kumazoe, Motofumi</creatorcontrib><creatorcontrib>Yamashita, Mai</creatorcontrib><creatorcontrib>Nakamura, Yuki</creatorcontrib><creatorcontrib>Takamatsu, Kanako</creatorcontrib><creatorcontrib>Bae, Jaehoon</creatorcontrib><creatorcontrib>Yamashita, Shuya</creatorcontrib><creatorcontrib>Yamada, Shuhei</creatorcontrib><creatorcontrib>Onda, Hiroaki</creatorcontrib><creatorcontrib>Nojiri, Takashi</creatorcontrib><creatorcontrib>Kangawa, Kenji</creatorcontrib><creatorcontrib>Tachibana, Hirofumi</creatorcontrib><title>Green Tea Polyphenol EGCG Upregulates Tollip Expression by Suppressing Elf-1 Expression</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>TLR signaling is critical to innate immune system regulation; however, aberrant TLR signaling is involved in several diseases, including insulin resistance, Alzheimer's disease, and tumor metastasis. Moreover, a recent study found that TLR-4 signaling pathway inhibition might be a target for the suppression of chronic inflammatory disorders. In this article, we show that the green tea polyphenol epigallocatechin-3-
-gallate (EGCG) increases the expression of Toll interacting protein, a strong inhibitor of TLR4 signaling, by suppressing the expression of E74-like ETS transcription factor 1 (Elf-1). A mechanistic study revealed that EGCG suppressed Elf-1 expression via protein phosphatase 2A/cyclic GMP (cGMP)-dependent mechanisms. We also confirmed that orally administered EGCG and a cGMP inducer upregulated Toll interacting protein expression, increased intracellular levels of cGMP in macrophages, and suppressed Elf-1 expression. These data support EGCG and a cGMP inducer as potential candidate suppressors of TLR4 signaling.</description><subject>Animals</subject><subject>Catechin - analogs & derivatives</subject><subject>Catechin - chemistry</subject><subject>Catechin - pharmacology</subject><subject>Cyclic GMP</subject><subject>Cyclic GMP - genetics</subject><subject>Cyclic GMP - immunology</subject><subject>Disease resistance</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - immunology</subject><subject>Epigallocatechin gallate</subject><subject>ETS protein</subject><subject>Green tea</subject><subject>Immune system</subject><subject>Inflammatory diseases</subject><subject>Innate immunity</subject><subject>Insulin</subject><subject>Intracellular levels</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - immunology</subject><subject>Macrophages</subject><subject>Male</subject><subject>Metastases</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - immunology</subject><subject>Oral administration</subject><subject>Phosphoprotein phosphatase</subject><subject>Protein phosphatase</subject><subject>Protein Phosphatase 2 - genetics</subject><subject>Protein Phosphatase 2 - immunology</subject><subject>Proteins</subject><subject>Second Messenger Systems - genetics</subject><subject>Second Messenger Systems - immunology</subject><subject>Signal transduction</subject><subject>Tea</subject><subject>Tea - chemistry</subject><subject>TLR4 protein</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - immunology</subject><subject>Toll-like receptors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - immunology</subject><subject>Up-Regulation - immunology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE1Lw0AQhhdRbK3ePcmCFy-psx_ZbI5SYhQKCrZ4DGkyW1M2H2YbsP_elbYinoaZeeZleAi5ZjCVIOP7TVXXQ9PaKVPANOcnZMzCEAKlQJ2SMQDnAYtUNCIXzm0AQAGX52TEdRxKrcMxeU97xIYuMKevrd11H-jjaJLOUrrselwPNt-io4vW2qqjyZefOVe1DV3t6NvQ7dtmTRNrAvZnf0nOTG4dXh3qhCwfk8XsKZi_pM-zh3lQSBFuA4wNN3GORYxlFIEsEKSIQJWixNzEK61LFIYzgJJxphlItSoE06IsI4nGiAm52-d2ffs5oNtmdeUKtDZvsB1cxmIpfSKPlUdv_6Gbdugb_52ntBRcecxTsKeKvnWuR5N1fVXn_S5jkP1Iz47Ss4N0f3JzCB5WNZa_B0fL4htSJ379</recordid><startdate>20171101</startdate><enddate>20171101</enddate><creator>Kumazoe, Motofumi</creator><creator>Yamashita, Mai</creator><creator>Nakamura, Yuki</creator><creator>Takamatsu, Kanako</creator><creator>Bae, Jaehoon</creator><creator>Yamashita, Shuya</creator><creator>Yamada, Shuhei</creator><creator>Onda, Hiroaki</creator><creator>Nojiri, Takashi</creator><creator>Kangawa, Kenji</creator><creator>Tachibana, Hirofumi</creator><general>American Association of Immunologists</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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20171101</creationdate><title>Green Tea Polyphenol EGCG Upregulates Tollip Expression by Suppressing Elf-1 Expression</title><author>Kumazoe, Motofumi ; Yamashita, Mai ; Nakamura, Yuki ; Takamatsu, Kanako ; Bae, Jaehoon ; Yamashita, Shuya ; Yamada, Shuhei ; Onda, Hiroaki ; Nojiri, Takashi ; Kangawa, Kenji ; Tachibana, Hirofumi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c435t-e9f2f9aec9ed7704ce043706d3deaf9b88de3f2100d12181046bc3183dd74eff3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Catechin - analogs & derivatives</topic><topic>Catechin - chemistry</topic><topic>Catechin - pharmacology</topic><topic>Cyclic GMP</topic><topic>Cyclic GMP - genetics</topic><topic>Cyclic GMP - immunology</topic><topic>Disease resistance</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - immunology</topic><topic>Epigallocatechin gallate</topic><topic>ETS protein</topic><topic>Green tea</topic><topic>Immune system</topic><topic>Inflammatory diseases</topic><topic>Innate immunity</topic><topic>Insulin</topic><topic>Intracellular levels</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - immunology</topic><topic>Macrophages</topic><topic>Male</topic><topic>Metastases</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - immunology</topic><topic>Oral administration</topic><topic>Phosphoprotein phosphatase</topic><topic>Protein phosphatase</topic><topic>Protein Phosphatase 2 - genetics</topic><topic>Protein Phosphatase 2 - immunology</topic><topic>Proteins</topic><topic>Second Messenger Systems - genetics</topic><topic>Second Messenger Systems - immunology</topic><topic>Signal transduction</topic><topic>Tea</topic><topic>Tea - chemistry</topic><topic>TLR4 protein</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - immunology</topic><topic>Toll-like receptors</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - immunology</topic><topic>Up-Regulation - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kumazoe, Motofumi</creatorcontrib><creatorcontrib>Yamashita, Mai</creatorcontrib><creatorcontrib>Nakamura, Yuki</creatorcontrib><creatorcontrib>Takamatsu, Kanako</creatorcontrib><creatorcontrib>Bae, Jaehoon</creatorcontrib><creatorcontrib>Yamashita, Shuya</creatorcontrib><creatorcontrib>Yamada, Shuhei</creatorcontrib><creatorcontrib>Onda, Hiroaki</creatorcontrib><creatorcontrib>Nojiri, Takashi</creatorcontrib><creatorcontrib>Kangawa, Kenji</creatorcontrib><creatorcontrib>Tachibana, Hirofumi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kumazoe, Motofumi</au><au>Yamashita, Mai</au><au>Nakamura, Yuki</au><au>Takamatsu, Kanako</au><au>Bae, Jaehoon</au><au>Yamashita, Shuya</au><au>Yamada, Shuhei</au><au>Onda, Hiroaki</au><au>Nojiri, Takashi</au><au>Kangawa, Kenji</au><au>Tachibana, Hirofumi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Green Tea Polyphenol EGCG Upregulates Tollip Expression by Suppressing Elf-1 Expression</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2017-11-01</date><risdate>2017</risdate><volume>199</volume><issue>9</issue><spage>3261</spage><epage>3269</epage><pages>3261-3269</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>TLR signaling is critical to innate immune system regulation; however, aberrant TLR signaling is involved in several diseases, including insulin resistance, Alzheimer's disease, and tumor metastasis. Moreover, a recent study found that TLR-4 signaling pathway inhibition might be a target for the suppression of chronic inflammatory disorders. In this article, we show that the green tea polyphenol epigallocatechin-3-
-gallate (EGCG) increases the expression of Toll interacting protein, a strong inhibitor of TLR4 signaling, by suppressing the expression of E74-like ETS transcription factor 1 (Elf-1). A mechanistic study revealed that EGCG suppressed Elf-1 expression via protein phosphatase 2A/cyclic GMP (cGMP)-dependent mechanisms. We also confirmed that orally administered EGCG and a cGMP inducer upregulated Toll interacting protein expression, increased intracellular levels of cGMP in macrophages, and suppressed Elf-1 expression. These data support EGCG and a cGMP inducer as potential candidate suppressors of TLR4 signaling.</abstract><cop>United States</cop><pub>American Association of Immunologists</pub><pmid>28954885</pmid><doi>10.4049/jimmunol.1601822</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Catechin - analogs & derivatives Catechin - chemistry Catechin - pharmacology Cyclic GMP Cyclic GMP - genetics Cyclic GMP - immunology Disease resistance DNA-Binding Proteins - genetics DNA-Binding Proteins - immunology Epigallocatechin gallate ETS protein Green tea Immune system Inflammatory diseases Innate immunity Insulin Intracellular levels Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - immunology Macrophages Male Metastases Mice Mice, Inbred BALB C Nuclear Proteins - genetics Nuclear Proteins - immunology Oral administration Phosphoprotein phosphatase Protein phosphatase Protein Phosphatase 2 - genetics Protein Phosphatase 2 - immunology Proteins Second Messenger Systems - genetics Second Messenger Systems - immunology Signal transduction Tea Tea - chemistry TLR4 protein Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - immunology Toll-like receptors Transcription Factors - genetics Transcription Factors - immunology Up-Regulation - immunology |
| title | Green Tea Polyphenol EGCG Upregulates Tollip Expression by Suppressing Elf-1 Expression |
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