Fibroblast growth factor (Fgf) 21 is a novel target gene of the aryl hydrocarbon receptor (AhR)
The toxic effects of dioxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), mainly through activation of the aryl hydrocarbon receptor (AhR) are well documented. Fibroblast growth factor (Fgf) 21 plays critical roles in metabolic adaptation to fasting by increasing lipid oxidation and ketogene...
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| Veröffentlicht in: | Toxicology and applied pharmacology 2014-07, Vol.278 (1), p.65-71 |
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| creator | Cheng, Xingguo Vispute, Saurabh G. Liu, Jie Cheng, Christine Kharitonenkov, Alexei Klaassen, Curtis D. |
| description | The toxic effects of dioxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), mainly through activation of the aryl hydrocarbon receptor (AhR) are well documented. Fibroblast growth factor (Fgf) 21 plays critical roles in metabolic adaptation to fasting by increasing lipid oxidation and ketogenesis in the liver. The present study was performed to determine whether activation of the AhR induces Fgf21 expression. In mouse liver, TCDD increased Fgf21 mRNA in both dose- and time-dependent manners. In addition, TCDD markedly increased Fgf21 mRNA expression in cultured mouse and human hepatocytes. Moreover, TCDD increased mRNA (in liver) and protein levels (in both liver and serum) of Fgf21 in wild-type mice, but not in AhR-null mice. Chromatin immunoprecipitation assays showed that TCDD increased AhR protein binding to the Fgf21 promoter (−105/+1 base pair). Fgf21-null mice administered 200μg/kg of TCDD died within 20days, whereas wild-type mice receiving the same treatment were still alive at one month after administration. This indicates that TCDD-induced Fgf21 expression protects against TCDD toxicity. Diethylhexylphthalate (DEHP) pretreatment attenuated TCDD-induced Fgf21 expression in mouse liver and white adipose tissue, which may explain a previous report that DEHP pretreatment decreases TCDD-induced wasting. In conclusion, Fgf21 appears to be a target gene of AhR-signaling pathway in mouse and human liver.
•TCDD induced Fgf21 expression at both mRNA and protein levels.•Fgf21 induction by TCDD is AhR-dependent.•DEHP attenuated TCDD-induced Fgf21 expression. |
| doi_str_mv | 10.1016/j.taap.2014.04.013 |
| format | Article |
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•TCDD induced Fgf21 expression at both mRNA and protein levels.•Fgf21 induction by TCDD is AhR-dependent.•DEHP attenuated TCDD-induced Fgf21 expression.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2014.04.013</identifier><identifier>PMID: 24769090</identifier><identifier>CODEN: TXAPA9</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; ADIPOSE TISSUE ; Adipose Tissue, White - drug effects ; Adipose Tissue, White - metabolism ; AhR ; Animals ; Basic Helix-Loop-Helix Transcription Factors - agonists ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Binding Sites ; Biological and medical sciences ; Cell Line ; DEHP ; Diethylhexyl Phthalate - pharmacology ; DIOXIN ; DNA ; Dose-Response Relationship, Drug ; ENZYMES ; Fgf21 ; Fibroblast Growth Factors - deficiency ; Fibroblast Growth Factors - genetics ; Fibroblast Growth Factors - metabolism ; FIBROBLASTS ; GENES ; GROWTH FACTORS ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Humans ; HYDROCARBONS ; LIVER ; Liver - drug effects ; Liver - metabolism ; LIVER CELLS ; Male ; Medical sciences ; MESSENGER-RNA ; MICE ; Mice, Inbred C57BL ; Mice, Knockout ; Polychlorinated Dibenzodioxins - toxicity ; Promoter Regions, Genetic ; RECEPTORS ; Receptors, Aryl Hydrocarbon - agonists ; Receptors, Aryl Hydrocarbon - metabolism ; RNA, Messenger - metabolism ; Signal Transduction - drug effects ; TCDD ; TIME DEPENDENCE ; Time Factors ; TOXICITY ; Toxicology ; Up-Regulation ; White adipose tissue</subject><ispartof>Toxicology and applied pharmacology, 2014-07, Vol.278 (1), p.65-71</ispartof><rights>2014 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2014 Elsevier Inc. All rights reserved.</rights><rights>2014 Elsevier Inc. All rights reserved. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c579t-ca8409e616bb1256c160277dffebd3517179910dc0621a2ace623970a8ca05183</citedby><cites>FETCH-LOGICAL-c579t-ca8409e616bb1256c160277dffebd3517179910dc0621a2ace623970a8ca05183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.taap.2014.04.013$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=29109265$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24769090$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/22439751$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheng, Xingguo</creatorcontrib><creatorcontrib>Vispute, Saurabh G.</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Cheng, Christine</creatorcontrib><creatorcontrib>Kharitonenkov, Alexei</creatorcontrib><creatorcontrib>Klaassen, Curtis D.</creatorcontrib><title>Fibroblast growth factor (Fgf) 21 is a novel target gene of the aryl hydrocarbon receptor (AhR)</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>The toxic effects of dioxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), mainly through activation of the aryl hydrocarbon receptor (AhR) are well documented. Fibroblast growth factor (Fgf) 21 plays critical roles in metabolic adaptation to fasting by increasing lipid oxidation and ketogenesis in the liver. The present study was performed to determine whether activation of the AhR induces Fgf21 expression. In mouse liver, TCDD increased Fgf21 mRNA in both dose- and time-dependent manners. In addition, TCDD markedly increased Fgf21 mRNA expression in cultured mouse and human hepatocytes. Moreover, TCDD increased mRNA (in liver) and protein levels (in both liver and serum) of Fgf21 in wild-type mice, but not in AhR-null mice. Chromatin immunoprecipitation assays showed that TCDD increased AhR protein binding to the Fgf21 promoter (−105/+1 base pair). Fgf21-null mice administered 200μg/kg of TCDD died within 20days, whereas wild-type mice receiving the same treatment were still alive at one month after administration. This indicates that TCDD-induced Fgf21 expression protects against TCDD toxicity. Diethylhexylphthalate (DEHP) pretreatment attenuated TCDD-induced Fgf21 expression in mouse liver and white adipose tissue, which may explain a previous report that DEHP pretreatment decreases TCDD-induced wasting. In conclusion, Fgf21 appears to be a target gene of AhR-signaling pathway in mouse and human liver.
•TCDD induced Fgf21 expression at both mRNA and protein levels.•Fgf21 induction by TCDD is AhR-dependent.•DEHP attenuated TCDD-induced Fgf21 expression.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>ADIPOSE TISSUE</subject><subject>Adipose Tissue, White - drug effects</subject><subject>Adipose Tissue, White - metabolism</subject><subject>AhR</subject><subject>Animals</subject><subject>Basic Helix-Loop-Helix Transcription Factors - agonists</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Binding Sites</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>DEHP</subject><subject>Diethylhexyl Phthalate - pharmacology</subject><subject>DIOXIN</subject><subject>DNA</subject><subject>Dose-Response Relationship, Drug</subject><subject>ENZYMES</subject><subject>Fgf21</subject><subject>Fibroblast Growth Factors - deficiency</subject><subject>Fibroblast Growth Factors - genetics</subject><subject>Fibroblast Growth Factors - metabolism</subject><subject>FIBROBLASTS</subject><subject>GENES</subject><subject>GROWTH FACTORS</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Humans</subject><subject>HYDROCARBONS</subject><subject>LIVER</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>LIVER CELLS</subject><subject>Male</subject><subject>Medical sciences</subject><subject>MESSENGER-RNA</subject><subject>MICE</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Polychlorinated Dibenzodioxins - toxicity</subject><subject>Promoter Regions, Genetic</subject><subject>RECEPTORS</subject><subject>Receptors, Aryl Hydrocarbon - agonists</subject><subject>Receptors, Aryl Hydrocarbon - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>TCDD</subject><subject>TIME DEPENDENCE</subject><subject>Time Factors</subject><subject>TOXICITY</subject><subject>Toxicology</subject><subject>Up-Regulation</subject><subject>White adipose tissue</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kdFrFDEQxoMo9qz-Az5IQIT2Yc-Z7G72AkUoxdNCQRAF30I2O3ubY7s5knjS_75Zr7b1pTCQh_zmm2_mY-wtwhIB5cftMhmzWwrAagm5sHzGFghKFlCW5XO2AKiwAFj9OmKvYtwCgKoqfMmORNVIBQoWTK9dG3w7mpj4Jvg_aeC9sckHfrLe9KdcIHeRGz75PY08mbChDNJE3Pc8DcRNuBn5cNMFb01o_cQDWdr9FTgfvp--Zi96M0Z6c_ces5_rzz8uvhZX375cXpxfFbZuVCqsWVWgSKJsWxS1tChBNE3X99R2ZY0NNkohdBakQCOMJSlK1YBZWQM1rspj9umgu_vdXlNnaUrBjHoX3HV2qL1x-v-fyQ164_c6j4V8jizw_iDgY3I6WpfIDtZPE9mkhajytBozJQ6UDT7GQP39BAQ9h6K3eg5Fz6FoyIVlbnr32Nt9y78UMvDhDjDRmrEPZrIuPnB5cyVknbmzA0f5kntHYfZJk6XOhdlm591TPm4BTDGpsw</recordid><startdate>20140701</startdate><enddate>20140701</enddate><creator>Cheng, Xingguo</creator><creator>Vispute, Saurabh G.</creator><creator>Liu, Jie</creator><creator>Cheng, Christine</creator><creator>Kharitonenkov, Alexei</creator><creator>Klaassen, Curtis D.</creator><general>Elsevier Inc</general><general>Elsevier</general><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>OTOTI</scope><scope>5PM</scope></search><sort><creationdate>20140701</creationdate><title>Fibroblast growth factor (Fgf) 21 is a novel target gene of the aryl hydrocarbon receptor (AhR)</title><author>Cheng, Xingguo ; Vispute, Saurabh G. ; Liu, Jie ; Cheng, Christine ; Kharitonenkov, Alexei ; Klaassen, Curtis D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c579t-ca8409e616bb1256c160277dffebd3517179910dc0621a2ace623970a8ca05183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>ADIPOSE TISSUE</topic><topic>Adipose Tissue, White - drug effects</topic><topic>Adipose Tissue, White - metabolism</topic><topic>AhR</topic><topic>Animals</topic><topic>Basic Helix-Loop-Helix Transcription Factors - agonists</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Binding Sites</topic><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>DEHP</topic><topic>Diethylhexyl Phthalate - pharmacology</topic><topic>DIOXIN</topic><topic>DNA</topic><topic>Dose-Response Relationship, Drug</topic><topic>ENZYMES</topic><topic>Fgf21</topic><topic>Fibroblast Growth Factors - deficiency</topic><topic>Fibroblast Growth Factors - genetics</topic><topic>Fibroblast Growth Factors - metabolism</topic><topic>FIBROBLASTS</topic><topic>GENES</topic><topic>GROWTH FACTORS</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>Humans</topic><topic>HYDROCARBONS</topic><topic>LIVER</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>LIVER CELLS</topic><topic>Male</topic><topic>Medical sciences</topic><topic>MESSENGER-RNA</topic><topic>MICE</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Polychlorinated Dibenzodioxins - toxicity</topic><topic>Promoter Regions, Genetic</topic><topic>RECEPTORS</topic><topic>Receptors, Aryl Hydrocarbon - agonists</topic><topic>Receptors, Aryl Hydrocarbon - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>TCDD</topic><topic>TIME DEPENDENCE</topic><topic>Time Factors</topic><topic>TOXICITY</topic><topic>Toxicology</topic><topic>Up-Regulation</topic><topic>White adipose tissue</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheng, Xingguo</creatorcontrib><creatorcontrib>Vispute, Saurabh G.</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Cheng, Christine</creatorcontrib><creatorcontrib>Kharitonenkov, Alexei</creatorcontrib><creatorcontrib>Klaassen, Curtis D.</creatorcontrib><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>OSTI.GOV</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheng, Xingguo</au><au>Vispute, Saurabh G.</au><au>Liu, Jie</au><au>Cheng, Christine</au><au>Kharitonenkov, Alexei</au><au>Klaassen, Curtis D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fibroblast growth factor (Fgf) 21 is a novel target gene of the aryl hydrocarbon receptor (AhR)</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2014-07-01</date><risdate>2014</risdate><volume>278</volume><issue>1</issue><spage>65</spage><epage>71</epage><pages>65-71</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>The toxic effects of dioxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), mainly through activation of the aryl hydrocarbon receptor (AhR) are well documented. Fibroblast growth factor (Fgf) 21 plays critical roles in metabolic adaptation to fasting by increasing lipid oxidation and ketogenesis in the liver. The present study was performed to determine whether activation of the AhR induces Fgf21 expression. In mouse liver, TCDD increased Fgf21 mRNA in both dose- and time-dependent manners. In addition, TCDD markedly increased Fgf21 mRNA expression in cultured mouse and human hepatocytes. Moreover, TCDD increased mRNA (in liver) and protein levels (in both liver and serum) of Fgf21 in wild-type mice, but not in AhR-null mice. Chromatin immunoprecipitation assays showed that TCDD increased AhR protein binding to the Fgf21 promoter (−105/+1 base pair). Fgf21-null mice administered 200μg/kg of TCDD died within 20days, whereas wild-type mice receiving the same treatment were still alive at one month after administration. This indicates that TCDD-induced Fgf21 expression protects against TCDD toxicity. Diethylhexylphthalate (DEHP) pretreatment attenuated TCDD-induced Fgf21 expression in mouse liver and white adipose tissue, which may explain a previous report that DEHP pretreatment decreases TCDD-induced wasting. In conclusion, Fgf21 appears to be a target gene of AhR-signaling pathway in mouse and human liver.
•TCDD induced Fgf21 expression at both mRNA and protein levels.•Fgf21 induction by TCDD is AhR-dependent.•DEHP attenuated TCDD-induced Fgf21 expression.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>24769090</pmid><doi>10.1016/j.taap.2014.04.013</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 60 APPLIED LIFE SCIENCES ADIPOSE TISSUE Adipose Tissue, White - drug effects Adipose Tissue, White - metabolism AhR Animals Basic Helix-Loop-Helix Transcription Factors - agonists Basic Helix-Loop-Helix Transcription Factors - metabolism Binding Sites Biological and medical sciences Cell Line DEHP Diethylhexyl Phthalate - pharmacology DIOXIN DNA Dose-Response Relationship, Drug ENZYMES Fgf21 Fibroblast Growth Factors - deficiency Fibroblast Growth Factors - genetics Fibroblast Growth Factors - metabolism FIBROBLASTS GENES GROWTH FACTORS Hepatocytes - drug effects Hepatocytes - metabolism Humans HYDROCARBONS LIVER Liver - drug effects Liver - metabolism LIVER CELLS Male Medical sciences MESSENGER-RNA MICE Mice, Inbred C57BL Mice, Knockout Polychlorinated Dibenzodioxins - toxicity Promoter Regions, Genetic RECEPTORS Receptors, Aryl Hydrocarbon - agonists Receptors, Aryl Hydrocarbon - metabolism RNA, Messenger - metabolism Signal Transduction - drug effects TCDD TIME DEPENDENCE Time Factors TOXICITY Toxicology Up-Regulation White adipose tissue |
| title | Fibroblast growth factor (Fgf) 21 is a novel target gene of the aryl hydrocarbon receptor (AhR) |
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