Induction of orphan nuclear receptor Nur77 gene expression and its role in cadmium-induced apoptosis in lung
Cadmium is an environmentally widely dispersed and highly toxic heavy metal that has been classified as a human carcinogen. Using the suppression subtractive hybridization technique, we identified previously 29 cadmium-inducible genes, primarily involved in inflammation, cell survival and apoptosis....
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| Veröffentlicht in: | Carcinogenesis (New York) 2004-08, Vol.25 (8), p.1467-1475 |
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| creator | Shin, Hye-Jin Lee, Byung-Hoon Yeo, Myeong Goo Oh, Seon-Hee Park, Jung-Duck Park, Kun-Koo Chung, Jin-Ho Moon, Chang-Kiu Lee, Mi-Ock |
| description | Cadmium is an environmentally widely dispersed and highly toxic heavy metal that has been classified as a human carcinogen. Using the suppression subtractive hybridization technique, we identified previously 29 cadmium-inducible genes, primarily involved in inflammation, cell survival and apoptosis. Among these genes, we are particularly interested in Nor-1, because this gene belongs to the Nur77 family, which plays a key role in the apoptotic processes of a variety of cells and tissues, including the lung. In the present study, we characterized the induction of the Nur77 family genes in the lungs after cadmium exposure. Nur77, Nor-1 and Nurr1 were all induced after cadmium treatment in a dose- and time-dependent manner in WI-38 and A549 lung cell lines. Treatment with inhibitors of signaling pathways, such as PD98059 and H89, almost completely blocked the expression of Nur77, indicating that the extracellular signal-regulated kinase and protein kinase A signaling pathways are important in cadmium-induced Nur77 expression. When a plasmid encoding dominant-negative Nur77 was transfected into A549 cells, cadmium-induced apoptotic changes, such as chromosomal condensation and Bax expression, were significantly reduced, suggesting that the expression of Nur77 plays an important role in cadmium-induced apoptosis. Furthermore, the number of apoptotic cells and the expression of Nur77 was increased in lung tissues collected from cadmium-treated (30 µmol/kg body wt) Wistar rats. Taken together, these results demonstrate that cadmium induces the expression of Nur77 family genes, leading to apoptosis in lung cells, which may cause pulmonary toxicity in response to cadmium exposure. |
| doi_str_mv | 10.1093/carcin/bgh135 |
| format | Article |
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Using the suppression subtractive hybridization technique, we identified previously 29 cadmium-inducible genes, primarily involved in inflammation, cell survival and apoptosis. Among these genes, we are particularly interested in Nor-1, because this gene belongs to the Nur77 family, which plays a key role in the apoptotic processes of a variety of cells and tissues, including the lung. In the present study, we characterized the induction of the Nur77 family genes in the lungs after cadmium exposure. Nur77, Nor-1 and Nurr1 were all induced after cadmium treatment in a dose- and time-dependent manner in WI-38 and A549 lung cell lines. Treatment with inhibitors of signaling pathways, such as PD98059 and H89, almost completely blocked the expression of Nur77, indicating that the extracellular signal-regulated kinase and protein kinase A signaling pathways are important in cadmium-induced Nur77 expression. When a plasmid encoding dominant-negative Nur77 was transfected into A549 cells, cadmium-induced apoptotic changes, such as chromosomal condensation and Bax expression, were significantly reduced, suggesting that the expression of Nur77 plays an important role in cadmium-induced apoptosis. Furthermore, the number of apoptotic cells and the expression of Nur77 was increased in lung tissues collected from cadmium-treated (30 µmol/kg body wt) Wistar rats. Taken together, these results demonstrate that cadmium induces the expression of Nur77 family genes, leading to apoptosis in lung cells, which may cause pulmonary toxicity in response to cadmium exposure.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/bgh135</identifier><identifier>PMID: 15016657</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>5-dimethylthiazol-2-yl)-2 ; 5-diphenyl tetrazolium bromide ; 6-diamidino-2-phenylindole ; Animals ; Apoptosis ; bcl-2-Associated X Protein ; Biological and medical sciences ; Cadmium - metabolism ; Carcinogenesis, carcinogens and anticarcinogens ; Cell Line, Tumor ; Cell Survival ; Chemical and industrial products toxicology. Toxic occupational diseases ; Cyclic AMP-Dependent Protein Kinases - metabolism ; DAPI ; DNA-Binding Proteins - biosynthesis ; Dose-Response Relationship, Drug ; Enzyme Inhibitors - pharmacology ; ERK ; extracellular signal-regulated kinase ; Female ; Flavonoids - pharmacology ; Gene Expression Regulation ; Genes, Reporter ; Humans ; Immunohistochemistry ; Inflammation ; Isoquinolines - pharmacology ; Lung - pathology ; MAPK ; Medical sciences ; Metals and various inorganic compounds ; mitogen-activated protein kinase ; Mitogen-Activated Protein Kinases - metabolism ; MTT ; NBRE ; Nuclear Receptor Subfamily 4, Group A, Member 1 ; Nucleic Acid Hybridization ; Nur77-binding response element ; PBMC ; PBS ; peripheral blood mononuclear cells ; phosphate-buffered saline ; PKA ; Plasmids - metabolism ; Precipitin Tests ; protein kinase A ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-bcl-2 ; Rats ; Rats, Wistar ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; Reverse Transcriptase Polymerase Chain Reaction ; RT–PCT ; Signal Transduction ; Sulfonamides ; T-cell receptor ; TCR ; Time Factors ; Toxicology ; Transcription Factors - biosynthesis ; Transfection ; Tumors</subject><ispartof>Carcinogenesis (New York), 2004-08, Vol.25 (8), p.1467-1475</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Aug 1, 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-5d8c7144103414ac3a7a57d246eee0a3a19c25e64f23817c6fc79e39dffc758d3</citedby><cites>FETCH-LOGICAL-c452t-5d8c7144103414ac3a7a57d246eee0a3a19c25e64f23817c6fc79e39dffc758d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16025769$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15016657$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shin, Hye-Jin</creatorcontrib><creatorcontrib>Lee, Byung-Hoon</creatorcontrib><creatorcontrib>Yeo, Myeong Goo</creatorcontrib><creatorcontrib>Oh, Seon-Hee</creatorcontrib><creatorcontrib>Park, Jung-Duck</creatorcontrib><creatorcontrib>Park, Kun-Koo</creatorcontrib><creatorcontrib>Chung, Jin-Ho</creatorcontrib><creatorcontrib>Moon, Chang-Kiu</creatorcontrib><creatorcontrib>Lee, Mi-Ock</creatorcontrib><title>Induction of orphan nuclear receptor Nur77 gene expression and its role in cadmium-induced apoptosis in lung</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Cadmium is an environmentally widely dispersed and highly toxic heavy metal that has been classified as a human carcinogen. Using the suppression subtractive hybridization technique, we identified previously 29 cadmium-inducible genes, primarily involved in inflammation, cell survival and apoptosis. Among these genes, we are particularly interested in Nor-1, because this gene belongs to the Nur77 family, which plays a key role in the apoptotic processes of a variety of cells and tissues, including the lung. In the present study, we characterized the induction of the Nur77 family genes in the lungs after cadmium exposure. Nur77, Nor-1 and Nurr1 were all induced after cadmium treatment in a dose- and time-dependent manner in WI-38 and A549 lung cell lines. Treatment with inhibitors of signaling pathways, such as PD98059 and H89, almost completely blocked the expression of Nur77, indicating that the extracellular signal-regulated kinase and protein kinase A signaling pathways are important in cadmium-induced Nur77 expression. When a plasmid encoding dominant-negative Nur77 was transfected into A549 cells, cadmium-induced apoptotic changes, such as chromosomal condensation and Bax expression, were significantly reduced, suggesting that the expression of Nur77 plays an important role in cadmium-induced apoptosis. Furthermore, the number of apoptotic cells and the expression of Nur77 was increased in lung tissues collected from cadmium-treated (30 µmol/kg body wt) Wistar rats. Taken together, these results demonstrate that cadmium induces the expression of Nur77 family genes, leading to apoptosis in lung cells, which may cause pulmonary toxicity in response to cadmium exposure.</description><subject>5-dimethylthiazol-2-yl)-2</subject><subject>5-diphenyl tetrazolium bromide</subject><subject>6-diamidino-2-phenylindole</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>bcl-2-Associated X Protein</subject><subject>Biological and medical sciences</subject><subject>Cadmium - metabolism</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>DAPI</subject><subject>DNA-Binding Proteins - biosynthesis</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>ERK</subject><subject>extracellular signal-regulated kinase</subject><subject>Female</subject><subject>Flavonoids - pharmacology</subject><subject>Gene Expression Regulation</subject><subject>Genes, Reporter</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Isoquinolines - pharmacology</subject><subject>Lung - pathology</subject><subject>MAPK</subject><subject>Medical sciences</subject><subject>Metals and various inorganic compounds</subject><subject>mitogen-activated protein kinase</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>MTT</subject><subject>NBRE</subject><subject>Nuclear Receptor Subfamily 4, Group A, Member 1</subject><subject>Nucleic Acid Hybridization</subject><subject>Nur77-binding response element</subject><subject>PBMC</subject><subject>PBS</subject><subject>peripheral blood mononuclear cells</subject><subject>phosphate-buffered saline</subject><subject>PKA</subject><subject>Plasmids - metabolism</subject><subject>Precipitin Tests</subject><subject>protein kinase A</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Cytoplasmic and Nuclear</subject><subject>Receptors, Steroid</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RT–PCT</subject><subject>Signal Transduction</subject><subject>Sulfonamides</subject><subject>T-cell receptor</subject><subject>TCR</subject><subject>Time Factors</subject><subject>Toxicology</subject><subject>Transcription Factors - biosynthesis</subject><subject>Transfection</subject><subject>Tumors</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkd1rFTEQxYNY7G310VcJgr5tm-9sHm2xH9BWEBXxJaTZ2dvU3WRNNtD-9-7lXrzg0xyY35wZ5iD0lpITSgw_9S77EE_v1w-UyxdoRYUiDaMteYlWhArecM7FIToq5ZEQqrg0r9AhlYtUUq_QcB276ueQIk49Tnl6cBHH6gdwGWfwMM0p47uatcZriIDhacpQymbAxQ6HueCcBsAhYu-6MdSxCRtL6LCb0jJdQtk0hxrXr9FB74YCb3b1GH2_-Pzt_Kq5-XJ5ff7ppvFCsrmRXes1FYISLqhwnjvtpO6YUABAHHfUeCZBiZ7xlmqveq8NcNP1i5Btx4_Rx63vlNOfCmW2YygehsFFSLVYagwzRIsFfP8f-JhqjsttllHDmaSqXaBmC_mcSsnQ2ymH0eVnS4ndZGC3GdhtBgv_bmda70fo9vTu6QvwYQe44t3QZxd9KHtOESa1MvvFoczw9K_v8m-rNNfSXv38Zb_-YBdK317aM_4XTuWgnA</recordid><startdate>20040801</startdate><enddate>20040801</enddate><creator>Shin, Hye-Jin</creator><creator>Lee, Byung-Hoon</creator><creator>Yeo, Myeong Goo</creator><creator>Oh, Seon-Hee</creator><creator>Park, Jung-Duck</creator><creator>Park, Kun-Koo</creator><creator>Chung, Jin-Ho</creator><creator>Moon, Chang-Kiu</creator><creator>Lee, Mi-Ock</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20040801</creationdate><title>Induction of orphan nuclear receptor Nur77 gene expression and its role in cadmium-induced apoptosis in lung</title><author>Shin, Hye-Jin ; Lee, Byung-Hoon ; Yeo, Myeong Goo ; Oh, Seon-Hee ; Park, Jung-Duck ; Park, Kun-Koo ; Chung, Jin-Ho ; Moon, Chang-Kiu ; Lee, Mi-Ock</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-5d8c7144103414ac3a7a57d246eee0a3a19c25e64f23817c6fc79e39dffc758d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>5-dimethylthiazol-2-yl)-2</topic><topic>5-diphenyl tetrazolium bromide</topic><topic>6-diamidino-2-phenylindole</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>bcl-2-Associated X Protein</topic><topic>Biological and medical sciences</topic><topic>Cadmium - metabolism</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>DAPI</topic><topic>DNA-Binding Proteins - biosynthesis</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>ERK</topic><topic>extracellular signal-regulated kinase</topic><topic>Female</topic><topic>Flavonoids - pharmacology</topic><topic>Gene Expression Regulation</topic><topic>Genes, Reporter</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Isoquinolines - pharmacology</topic><topic>Lung - pathology</topic><topic>MAPK</topic><topic>Medical sciences</topic><topic>Metals and various inorganic compounds</topic><topic>mitogen-activated protein kinase</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>MTT</topic><topic>NBRE</topic><topic>Nuclear Receptor Subfamily 4, Group A, Member 1</topic><topic>Nucleic Acid Hybridization</topic><topic>Nur77-binding response element</topic><topic>PBMC</topic><topic>PBS</topic><topic>peripheral blood mononuclear cells</topic><topic>phosphate-buffered saline</topic><topic>PKA</topic><topic>Plasmids - metabolism</topic><topic>Precipitin Tests</topic><topic>protein kinase A</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Cytoplasmic and Nuclear</topic><topic>Receptors, Steroid</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RT–PCT</topic><topic>Signal Transduction</topic><topic>Sulfonamides</topic><topic>T-cell receptor</topic><topic>TCR</topic><topic>Time Factors</topic><topic>Toxicology</topic><topic>Transcription Factors - biosynthesis</topic><topic>Transfection</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shin, Hye-Jin</creatorcontrib><creatorcontrib>Lee, Byung-Hoon</creatorcontrib><creatorcontrib>Yeo, Myeong Goo</creatorcontrib><creatorcontrib>Oh, Seon-Hee</creatorcontrib><creatorcontrib>Park, Jung-Duck</creatorcontrib><creatorcontrib>Park, Kun-Koo</creatorcontrib><creatorcontrib>Chung, Jin-Ho</creatorcontrib><creatorcontrib>Moon, Chang-Kiu</creatorcontrib><creatorcontrib>Lee, Mi-Ock</creatorcontrib><collection>Istex</collection><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>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shin, Hye-Jin</au><au>Lee, Byung-Hoon</au><au>Yeo, Myeong Goo</au><au>Oh, Seon-Hee</au><au>Park, Jung-Duck</au><au>Park, Kun-Koo</au><au>Chung, Jin-Ho</au><au>Moon, Chang-Kiu</au><au>Lee, Mi-Ock</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction of orphan nuclear receptor Nur77 gene expression and its role in cadmium-induced apoptosis in lung</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2004-08-01</date><risdate>2004</risdate><volume>25</volume><issue>8</issue><spage>1467</spage><epage>1475</epage><pages>1467-1475</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>Cadmium is an environmentally widely dispersed and highly toxic heavy metal that has been classified as a human carcinogen. Using the suppression subtractive hybridization technique, we identified previously 29 cadmium-inducible genes, primarily involved in inflammation, cell survival and apoptosis. Among these genes, we are particularly interested in Nor-1, because this gene belongs to the Nur77 family, which plays a key role in the apoptotic processes of a variety of cells and tissues, including the lung. In the present study, we characterized the induction of the Nur77 family genes in the lungs after cadmium exposure. Nur77, Nor-1 and Nurr1 were all induced after cadmium treatment in a dose- and time-dependent manner in WI-38 and A549 lung cell lines. Treatment with inhibitors of signaling pathways, such as PD98059 and H89, almost completely blocked the expression of Nur77, indicating that the extracellular signal-regulated kinase and protein kinase A signaling pathways are important in cadmium-induced Nur77 expression. When a plasmid encoding dominant-negative Nur77 was transfected into A549 cells, cadmium-induced apoptotic changes, such as chromosomal condensation and Bax expression, were significantly reduced, suggesting that the expression of Nur77 plays an important role in cadmium-induced apoptosis. Furthermore, the number of apoptotic cells and the expression of Nur77 was increased in lung tissues collected from cadmium-treated (30 µmol/kg body wt) Wistar rats. Taken together, these results demonstrate that cadmium induces the expression of Nur77 family genes, leading to apoptosis in lung cells, which may cause pulmonary toxicity in response to cadmium exposure.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>15016657</pmid><doi>10.1093/carcin/bgh135</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 5-dimethylthiazol-2-yl)-2 5-diphenyl tetrazolium bromide 6-diamidino-2-phenylindole Animals Apoptosis bcl-2-Associated X Protein Biological and medical sciences Cadmium - metabolism Carcinogenesis, carcinogens and anticarcinogens Cell Line, Tumor Cell Survival Chemical and industrial products toxicology. Toxic occupational diseases Cyclic AMP-Dependent Protein Kinases - metabolism DAPI DNA-Binding Proteins - biosynthesis Dose-Response Relationship, Drug Enzyme Inhibitors - pharmacology ERK extracellular signal-regulated kinase Female Flavonoids - pharmacology Gene Expression Regulation Genes, Reporter Humans Immunohistochemistry Inflammation Isoquinolines - pharmacology Lung - pathology MAPK Medical sciences Metals and various inorganic compounds mitogen-activated protein kinase Mitogen-Activated Protein Kinases - metabolism MTT NBRE Nuclear Receptor Subfamily 4, Group A, Member 1 Nucleic Acid Hybridization Nur77-binding response element PBMC PBS peripheral blood mononuclear cells phosphate-buffered saline PKA Plasmids - metabolism Precipitin Tests protein kinase A Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 Rats Rats, Wistar Receptors, Cytoplasmic and Nuclear Receptors, Steroid Reverse Transcriptase Polymerase Chain Reaction RT–PCT Signal Transduction Sulfonamides T-cell receptor TCR Time Factors Toxicology Transcription Factors - biosynthesis Transfection Tumors |
| title | Induction of orphan nuclear receptor Nur77 gene expression and its role in cadmium-induced apoptosis in lung |
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