GPBAR1/TGR5 mediates bile acid-induced cytokine expression in murine Kupffer cells
GPBAR1/TGR5 is a novel plasma membrane-bound G protein-coupled bile acid (BA) receptor. BAs are known to induce the expression of inflammatory cytokines in the liver with unknown mechanism. Here we show that without other external stimuli, TGR5 activation alone induced the expression of interleukin...
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| Veröffentlicht in: | PloS one 2014-04, Vol.9 (4), p.e93567 |
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| creator | Lou, Guiyu Ma, Xiaoxiao Fu, Xianghui Meng, Zhipeng Zhang, Wenyu Wang, Yan-Dong Van Ness, Carl Yu, Donna Xu, Rongzhen Huang, Wendong |
| description | GPBAR1/TGR5 is a novel plasma membrane-bound G protein-coupled bile acid (BA) receptor. BAs are known to induce the expression of inflammatory cytokines in the liver with unknown mechanism. Here we show that without other external stimuli, TGR5 activation alone induced the expression of interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) in murine macrophage cell line RAW264.7 or murine Kupffer cells. The TGR5-mediated increase of pro-inflammatory cytokine expression was suppressed by JNK inhibition. Moreover, the induced pro-inflammatory cytokine expression in mouse liver by 1% cholic acid (CA) diet was blunted in JNK-/- mice. TGR5 activation by its ligands enhanced the phosphorylation levels, DNA-binding and trans-activities of c-Jun and ATF2 transcription factors. Finally, the induced pro-inflammatory cytokine expression in Kupffer cells by TGR5 activation correlated with the suppression of Cholesterol 7α-hydroxylase (Cyp7a1) expression in murine hepatocytes. These results suggest that TGR5 mediates the BA-induced pro-inflammatory cytokine production in murine Kupffer cells through JNK-dependent pathway. This novel role of TGR5 may correlate to the suppression of Cyp7a1 expression in hepatocytes and contribute to the delicate BA feedback regulation. |
| doi_str_mv | 10.1371/journal.pone.0093567 |
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BAs are known to induce the expression of inflammatory cytokines in the liver with unknown mechanism. Here we show that without other external stimuli, TGR5 activation alone induced the expression of interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) in murine macrophage cell line RAW264.7 or murine Kupffer cells. The TGR5-mediated increase of pro-inflammatory cytokine expression was suppressed by JNK inhibition. Moreover, the induced pro-inflammatory cytokine expression in mouse liver by 1% cholic acid (CA) diet was blunted in JNK-/- mice. TGR5 activation by its ligands enhanced the phosphorylation levels, DNA-binding and trans-activities of c-Jun and ATF2 transcription factors. Finally, the induced pro-inflammatory cytokine expression in Kupffer cells by TGR5 activation correlated with the suppression of Cholesterol 7α-hydroxylase (Cyp7a1) expression in murine hepatocytes. These results suggest that TGR5 mediates the BA-induced pro-inflammatory cytokine production in murine Kupffer cells through JNK-dependent pathway. This novel role of TGR5 may correlate to the suppression of Cyp7a1 expression in hepatocytes and contribute to the delicate BA feedback regulation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0093567</identifier><identifier>PMID: 24755711</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acids ; Activating Transcription Factor 2 - metabolism ; Activation ; Analysis ; Animals ; Bile ; Bile Acids and Salts - pharmacology ; Biology and Life Sciences ; c-Jun protein ; Cell Line ; Chemical properties ; Cholesterol ; Cholesterol 7-alpha-Hydroxylase - genetics ; Cholesterol 7-alpha-Hydroxylase - metabolism ; Cholic acid ; Culture Media - pharmacology ; Cytokines ; Cytokines - genetics ; Cytokines - metabolism ; Deoxycholic acid ; Deoxyribonucleic acid ; DNA ; External stimuli ; G proteins ; Gene Expression Regulation - drug effects ; HEK293 Cells ; Hepatocytes ; Hepatocytes - drug effects ; Hepatocytes - enzymology ; Humans ; Hydroxylase ; IL-1β ; Inflammation ; Inflammation Mediators - metabolism ; Interleukins ; JNK Mitogen-Activated Protein Kinases - metabolism ; Kinases ; Kupffer cells ; Kupffer Cells - drug effects ; Kupffer Cells - metabolism ; Liver ; Liver - cytology ; Liver - enzymology ; Macrophages ; Membrane proteins ; Mice, Inbred C57BL ; Oleanolic Acid - pharmacology ; Phosphorylation ; Phosphorylation - drug effects ; Promoter Regions, Genetic - genetics ; Protein binding ; Proto-Oncogene Proteins c-jun - metabolism ; Receptors, G-Protein-Coupled - metabolism ; Research and Analysis Methods ; Rodents ; Transcription factors ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - genetics ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>PloS one, 2014-04, Vol.9 (4), p.e93567</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Lou et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Lou et al 2014 Lou et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-af895bb70d44d06362966d00bf3d149f66b1a4c03e6918eec1656fac737d6783</citedby><cites>FETCH-LOGICAL-c758t-af895bb70d44d06362966d00bf3d149f66b1a4c03e6918eec1656fac737d6783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3995640/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3995640/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24755711$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lou, Guiyu</creatorcontrib><creatorcontrib>Ma, Xiaoxiao</creatorcontrib><creatorcontrib>Fu, Xianghui</creatorcontrib><creatorcontrib>Meng, Zhipeng</creatorcontrib><creatorcontrib>Zhang, Wenyu</creatorcontrib><creatorcontrib>Wang, Yan-Dong</creatorcontrib><creatorcontrib>Van Ness, Carl</creatorcontrib><creatorcontrib>Yu, Donna</creatorcontrib><creatorcontrib>Xu, Rongzhen</creatorcontrib><creatorcontrib>Huang, Wendong</creatorcontrib><title>GPBAR1/TGR5 mediates bile acid-induced cytokine expression in murine Kupffer cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>GPBAR1/TGR5 is a novel plasma membrane-bound G protein-coupled bile acid (BA) receptor. BAs are known to induce the expression of inflammatory cytokines in the liver with unknown mechanism. Here we show that without other external stimuli, TGR5 activation alone induced the expression of interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) in murine macrophage cell line RAW264.7 or murine Kupffer cells. The TGR5-mediated increase of pro-inflammatory cytokine expression was suppressed by JNK inhibition. Moreover, the induced pro-inflammatory cytokine expression in mouse liver by 1% cholic acid (CA) diet was blunted in JNK-/- mice. TGR5 activation by its ligands enhanced the phosphorylation levels, DNA-binding and trans-activities of c-Jun and ATF2 transcription factors. Finally, the induced pro-inflammatory cytokine expression in Kupffer cells by TGR5 activation correlated with the suppression of Cholesterol 7α-hydroxylase (Cyp7a1) expression in murine hepatocytes. These results suggest that TGR5 mediates the BA-induced pro-inflammatory cytokine production in murine Kupffer cells through JNK-dependent pathway. This novel role of TGR5 may correlate to the suppression of Cyp7a1 expression in hepatocytes and contribute to the delicate BA feedback regulation.</description><subject>Acids</subject><subject>Activating Transcription Factor 2 - metabolism</subject><subject>Activation</subject><subject>Analysis</subject><subject>Animals</subject><subject>Bile</subject><subject>Bile Acids and Salts - pharmacology</subject><subject>Biology and Life Sciences</subject><subject>c-Jun protein</subject><subject>Cell Line</subject><subject>Chemical properties</subject><subject>Cholesterol</subject><subject>Cholesterol 7-alpha-Hydroxylase - genetics</subject><subject>Cholesterol 7-alpha-Hydroxylase - metabolism</subject><subject>Cholic acid</subject><subject>Culture Media - pharmacology</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Deoxycholic acid</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>External stimuli</subject><subject>G proteins</subject><subject>Gene Expression Regulation - drug effects</subject><subject>HEK293 Cells</subject><subject>Hepatocytes</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - enzymology</subject><subject>Humans</subject><subject>Hydroxylase</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukins</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Kinases</subject><subject>Kupffer cells</subject><subject>Kupffer Cells - drug effects</subject><subject>Kupffer Cells - metabolism</subject><subject>Liver</subject><subject>Liver - cytology</subject><subject>Liver - enzymology</subject><subject>Macrophages</subject><subject>Membrane proteins</subject><subject>Mice, Inbred C57BL</subject><subject>Oleanolic Acid - pharmacology</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Protein binding</subject><subject>Proto-Oncogene Proteins c-jun - metabolism</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Research and Analysis Methods</subject><subject>Rodents</subject><subject>Transcription factors</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLguBFZ_PRfPRGGBcdBxdWxsHbkOZjJmOnqUkru__ejNNdpqAguUhInvPm8J43y15CMIOYwcudH0Irm1nnWzMDoMKEskfZOawwKigC-PHJ-Sx7FuMOAII5pU-zM1QyQhiE59lq8fXDfAUv14sVyfdGO9mbmNeuMblUTheu1YMyOld3vf_hWpOb2y6YGJ1vc9fm-yEcLr8MnbUm5Mo0TXyePbGyiebFuF9k608f11efi-ubxfJqfl0oRnhfSMsrUtcM6LLUgGKKKko1ALXFGpaVpbSGslQAG1pBboyClFArFcNMU8bxRfb6KNs1PorRjSgggbxkgDGUiOWR0F7uRBfcXoY74aUTfy582AgZeqcaI6jkWlcWEU5RiSTglFUo_U04UARpmLTej78NdbJJmbYPspmITl9atxUb_0vgqiK0BEngzSgQ_M_BxP4fLY_URqauXGt9ElN7F5WY4zQzjjgtEzX7C5WWNnunUh5smt-04N2kIDG9ue03cohRLL-t_p-9-T5l356wWyObfht9M_QpHnEKlkdQBR9jMPbBOQjEIc73bohDnMUY51T26tT1h6L7_OLfP4Ttwg</recordid><startdate>20140401</startdate><enddate>20140401</enddate><creator>Lou, Guiyu</creator><creator>Ma, Xiaoxiao</creator><creator>Fu, Xianghui</creator><creator>Meng, Zhipeng</creator><creator>Zhang, Wenyu</creator><creator>Wang, Yan-Dong</creator><creator>Van Ness, Carl</creator><creator>Yu, Donna</creator><creator>Xu, Rongzhen</creator><creator>Huang, Wendong</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140401</creationdate><title>GPBAR1/TGR5 mediates bile acid-induced cytokine expression in murine Kupffer cells</title><author>Lou, Guiyu ; Ma, Xiaoxiao ; Fu, Xianghui ; Meng, Zhipeng ; Zhang, Wenyu ; Wang, Yan-Dong ; Van Ness, Carl ; Yu, Donna ; Xu, Rongzhen ; Huang, Wendong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-af895bb70d44d06362966d00bf3d149f66b1a4c03e6918eec1656fac737d6783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acids</topic><topic>Activating Transcription Factor 2 - metabolism</topic><topic>Activation</topic><topic>Analysis</topic><topic>Animals</topic><topic>Bile</topic><topic>Bile Acids and Salts - pharmacology</topic><topic>Biology and Life Sciences</topic><topic>c-Jun protein</topic><topic>Cell Line</topic><topic>Chemical properties</topic><topic>Cholesterol</topic><topic>Cholesterol 7-alpha-Hydroxylase - genetics</topic><topic>Cholesterol 7-alpha-Hydroxylase - metabolism</topic><topic>Cholic acid</topic><topic>Culture Media - pharmacology</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Deoxycholic acid</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>External stimuli</topic><topic>G proteins</topic><topic>Gene Expression Regulation - drug effects</topic><topic>HEK293 Cells</topic><topic>Hepatocytes</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - enzymology</topic><topic>Humans</topic><topic>Hydroxylase</topic><topic>IL-1β</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukins</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Kinases</topic><topic>Kupffer cells</topic><topic>Kupffer Cells - drug effects</topic><topic>Kupffer Cells - metabolism</topic><topic>Liver</topic><topic>Liver - cytology</topic><topic>Liver - enzymology</topic><topic>Macrophages</topic><topic>Membrane proteins</topic><topic>Mice, Inbred C57BL</topic><topic>Oleanolic Acid - pharmacology</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Protein binding</topic><topic>Proto-Oncogene Proteins c-jun - metabolism</topic><topic>Receptors, G-Protein-Coupled - metabolism</topic><topic>Research and Analysis Methods</topic><topic>Rodents</topic><topic>Transcription factors</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lou, Guiyu</creatorcontrib><creatorcontrib>Ma, Xiaoxiao</creatorcontrib><creatorcontrib>Fu, Xianghui</creatorcontrib><creatorcontrib>Meng, Zhipeng</creatorcontrib><creatorcontrib>Zhang, Wenyu</creatorcontrib><creatorcontrib>Wang, Yan-Dong</creatorcontrib><creatorcontrib>Van Ness, Carl</creatorcontrib><creatorcontrib>Yu, Donna</creatorcontrib><creatorcontrib>Xu, Rongzhen</creatorcontrib><creatorcontrib>Huang, Wendong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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BAs are known to induce the expression of inflammatory cytokines in the liver with unknown mechanism. Here we show that without other external stimuli, TGR5 activation alone induced the expression of interleukin 1β (IL-1β) and tumor necrosis factor-α (TNF-α) in murine macrophage cell line RAW264.7 or murine Kupffer cells. The TGR5-mediated increase of pro-inflammatory cytokine expression was suppressed by JNK inhibition. Moreover, the induced pro-inflammatory cytokine expression in mouse liver by 1% cholic acid (CA) diet was blunted in JNK-/- mice. TGR5 activation by its ligands enhanced the phosphorylation levels, DNA-binding and trans-activities of c-Jun and ATF2 transcription factors. Finally, the induced pro-inflammatory cytokine expression in Kupffer cells by TGR5 activation correlated with the suppression of Cholesterol 7α-hydroxylase (Cyp7a1) expression in murine hepatocytes. These results suggest that TGR5 mediates the BA-induced pro-inflammatory cytokine production in murine Kupffer cells through JNK-dependent pathway. This novel role of TGR5 may correlate to the suppression of Cyp7a1 expression in hepatocytes and contribute to the delicate BA feedback regulation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24755711</pmid><doi>10.1371/journal.pone.0093567</doi><oa>free_for_read</oa></addata></record> |
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| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Acids Activating Transcription Factor 2 - metabolism Activation Analysis Animals Bile Bile Acids and Salts - pharmacology Biology and Life Sciences c-Jun protein Cell Line Chemical properties Cholesterol Cholesterol 7-alpha-Hydroxylase - genetics Cholesterol 7-alpha-Hydroxylase - metabolism Cholic acid Culture Media - pharmacology Cytokines Cytokines - genetics Cytokines - metabolism Deoxycholic acid Deoxyribonucleic acid DNA External stimuli G proteins Gene Expression Regulation - drug effects HEK293 Cells Hepatocytes Hepatocytes - drug effects Hepatocytes - enzymology Humans Hydroxylase IL-1β Inflammation Inflammation Mediators - metabolism Interleukins JNK Mitogen-Activated Protein Kinases - metabolism Kinases Kupffer cells Kupffer Cells - drug effects Kupffer Cells - metabolism Liver Liver - cytology Liver - enzymology Macrophages Membrane proteins Mice, Inbred C57BL Oleanolic Acid - pharmacology Phosphorylation Phosphorylation - drug effects Promoter Regions, Genetic - genetics Protein binding Proto-Oncogene Proteins c-jun - metabolism Receptors, G-Protein-Coupled - metabolism Research and Analysis Methods Rodents Transcription factors Tumor necrosis factor Tumor Necrosis Factor-alpha - genetics Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | GPBAR1/TGR5 mediates bile acid-induced cytokine expression in murine Kupffer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T21%3A30%3A42IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=GPBAR1/TGR5%20mediates%20bile%20acid-induced%20cytokine%20expression%20in%20murine%20Kupffer%20cells&rft.jtitle=PloS%20one&rft.au=Lou,%20Guiyu&rft.date=2014-04-01&rft.volume=9&rft.issue=4&rft.spage=e93567&rft.pages=e93567-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0093567&rft_dat=%3Cgale_plos_%3EA375582864%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1518470772&rft_id=info:pmid/24755711&rft_galeid=A375582864&rft_doaj_id=oai_doaj_org_article_6a8dd9f2586242a086792c03580c52d1&rfr_iscdi=true |