Global Gene Expression Profiling of Dimethylnitrosamine-Induced Liver Fibrosis: From Pathological and Biochemical Data to Microarray Analysis
The development of hepatocellular carcinoma (HCC) is generally preceded by cirrhosis, which occurs at the end stage of fibrosis. This is a common and potentially lethal problem of chronic liver disease in Asia. The development of microarrays permits us to monitor transcriptomes on a genome-wide scal...
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| Veröffentlicht in: | Gene expression 2006-01, Vol.13 (2), p.107-132 |
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| creator | SU, LI-JEN HSU, SHIH-LAN YANG, JYH-SHYUE TSENG, HUEI-HUN HUANG, SHIU-FENG HUANG, AND CHI-YING F. |
| description | The development of hepatocellular carcinoma (HCC) is generally preceded by cirrhosis, which occurs at the end stage of fibrosis. This is a common and potentially lethal problem of chronic liver disease in Asia. The development of microarrays permits us to monitor transcriptomes on a
genome-wide scale; this has dramatically speeded up a comprehensive understanding of the disease process. Here we used dimethylnitrosamine (DMN), a nongenotoxic hepatotoxin, to induce rat necroinflammatory and hepatic fibrosis. During the 6-week time course, histopathological, biochemical,
and quantitative RT-PCR analyses confirmed the incidence of necroinflammatory and hepatic fibrosis in this established rat model system. Using the Affymetrix microarray chip, 256 differentially expressed genes were identified from the liver injury samples. Hierarchical clustering of gene expression
using a gene ontology database allowed the identification of several stage-specific characters and functionally related clusters that encode proteins related to metabolism, cell growth/maintenance, and response to external challenge. Among these genes, we classified 44 potential necroinflammatory-related
genes and 62 potential fibrosis-related markers or drug targets based on histopathological scores. We also compared the results with other data on well-known markers and various other microarray datasets that are available. In conclusion, we believe that the molecular picture of necroinflammatory
and hepatic fibrosis from this study may provide novel biological insights into the development of early liver damage molecular classifiers than can be used for basic research and in clinical applications. A public accessible website is available at http://LiverFibrosis.nchc.org.tw:8080/LF. |
| doi_str_mv | 10.3727/000000006783991872 |
| format | Article |
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genome-wide scale; this has dramatically speeded up a comprehensive understanding of the disease process. Here we used dimethylnitrosamine (DMN), a nongenotoxic hepatotoxin, to induce rat necroinflammatory and hepatic fibrosis. During the 6-week time course, histopathological, biochemical,
and quantitative RT-PCR analyses confirmed the incidence of necroinflammatory and hepatic fibrosis in this established rat model system. Using the Affymetrix microarray chip, 256 differentially expressed genes were identified from the liver injury samples. Hierarchical clustering of gene expression
using a gene ontology database allowed the identification of several stage-specific characters and functionally related clusters that encode proteins related to metabolism, cell growth/maintenance, and response to external challenge. Among these genes, we classified 44 potential necroinflammatory-related
genes and 62 potential fibrosis-related markers or drug targets based on histopathological scores. We also compared the results with other data on well-known markers and various other microarray datasets that are available. In conclusion, we believe that the molecular picture of necroinflammatory
and hepatic fibrosis from this study may provide novel biological insights into the development of early liver damage molecular classifiers than can be used for basic research and in clinical applications. A public accessible website is available at http://LiverFibrosis.nchc.org.tw:8080/LF.</description><identifier>ISSN: 1052-2166</identifier><identifier>EISSN: 1555-3884</identifier><identifier>DOI: 10.3727/000000006783991872</identifier><identifier>PMID: 17017125</identifier><language>eng</language><publisher>Elmsford, NY: Cognizant Communication Corporation</publisher><subject>Animals ; Antibodies ; Biochemical Data ; Biomarkers ; Cirrhosis ; Cluster analysis ; Clustering ; Dimethylnitrosamine ; Dimethylnitrosamine - toxicity ; Disease Models, Animal ; DNA microarrays ; Fibrosis ; Gene expression ; Gene Expression Profiling ; Genes ; Genomes ; Hepatitis ; Hepatocellular carcinoma ; Hepatotoxicity ; Histopathology ; Liver ; Liver - pathology ; Liver cancer ; Liver cirrhosis ; Liver Cirrhosis - chemically induced ; Liver Cirrhosis - genetics ; Liver Cirrhosis - metabolism ; Liver Cirrhosis - pathology ; Liver diseases ; Male ; Microarray ; N-Nitrosodimethylamine ; Necroinflammatory ; Oligonucleotide Array Sequence Analysis ; Phosphatase ; Polymerase Chain Reaction ; Quantitative RT-PCR ; Rats ; Rats, Sprague-Dawley ; Reference Values ; Risk factors ; Software ; Spp1 ; Tgfb1 ; Therapeutic targets ; Timp1 ; Transcriptomes</subject><ispartof>Gene expression, 2006-01, Vol.13 (2), p.107-132</ispartof><rights>Copyright Xia & He Publishing 2006</rights><rights>Copyright © 2006 Cognizant Comm. Corp. 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c584t-d7c2e1213bd5008bbb76cbcf3dc111b0853ed9ddf09c51c231fcb5632596d0993</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6032472/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/3054906042?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,21367,27901,27902,33721,33722,43781,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17017125$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SU, LI-JEN</creatorcontrib><creatorcontrib>HSU, SHIH-LAN</creatorcontrib><creatorcontrib>YANG, JYH-SHYUE</creatorcontrib><creatorcontrib>TSENG, HUEI-HUN</creatorcontrib><creatorcontrib>HUANG, SHIU-FENG</creatorcontrib><creatorcontrib>HUANG, AND CHI-YING F.</creatorcontrib><title>Global Gene Expression Profiling of Dimethylnitrosamine-Induced Liver Fibrosis: From Pathological and Biochemical Data to Microarray Analysis</title><title>Gene expression</title><addtitle>ge</addtitle><addtitle>Gene Expr</addtitle><description>The development of hepatocellular carcinoma (HCC) is generally preceded by cirrhosis, which occurs at the end stage of fibrosis. This is a common and potentially lethal problem of chronic liver disease in Asia. The development of microarrays permits us to monitor transcriptomes on a
genome-wide scale; this has dramatically speeded up a comprehensive understanding of the disease process. Here we used dimethylnitrosamine (DMN), a nongenotoxic hepatotoxin, to induce rat necroinflammatory and hepatic fibrosis. During the 6-week time course, histopathological, biochemical,
and quantitative RT-PCR analyses confirmed the incidence of necroinflammatory and hepatic fibrosis in this established rat model system. Using the Affymetrix microarray chip, 256 differentially expressed genes were identified from the liver injury samples. Hierarchical clustering of gene expression
using a gene ontology database allowed the identification of several stage-specific characters and functionally related clusters that encode proteins related to metabolism, cell growth/maintenance, and response to external challenge. Among these genes, we classified 44 potential necroinflammatory-related
genes and 62 potential fibrosis-related markers or drug targets based on histopathological scores. We also compared the results with other data on well-known markers and various other microarray datasets that are available. In conclusion, we believe that the molecular picture of necroinflammatory
and hepatic fibrosis from this study may provide novel biological insights into the development of early liver damage molecular classifiers than can be used for basic research and in clinical applications. A public accessible website is available at http://LiverFibrosis.nchc.org.tw:8080/LF.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Biochemical Data</subject><subject>Biomarkers</subject><subject>Cirrhosis</subject><subject>Cluster analysis</subject><subject>Clustering</subject><subject>Dimethylnitrosamine</subject><subject>Dimethylnitrosamine - toxicity</subject><subject>Disease Models, Animal</subject><subject>DNA microarrays</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Genes</subject><subject>Genomes</subject><subject>Hepatitis</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatotoxicity</subject><subject>Histopathology</subject><subject>Liver</subject><subject>Liver - pathology</subject><subject>Liver cancer</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - chemically induced</subject><subject>Liver Cirrhosis - genetics</subject><subject>Liver Cirrhosis - metabolism</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver diseases</subject><subject>Male</subject><subject>Microarray</subject><subject>N-Nitrosodimethylamine</subject><subject>Necroinflammatory</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Phosphatase</subject><subject>Polymerase Chain Reaction</subject><subject>Quantitative RT-PCR</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reference Values</subject><subject>Risk factors</subject><subject>Software</subject><subject>Spp1</subject><subject>Tgfb1</subject><subject>Therapeutic targets</subject><subject>Timp1</subject><subject>Transcriptomes</subject><issn>1052-2166</issn><issn>1555-3884</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFUk1v1DAQjRCIlsIf4IAsIXEL-GPtJByQSttdKm1FD3C2HNvJunLsxXZWLP-B_4zDBhboAV881rx582b8iuI5gq9Jhas3cD6sqknToLrCD4pTRCktSV0vHuYYUlxixNhJ8STGOwgxbGr8uDhBFUQVwvS0-L6yvhUWrLTT4OrrNugYjXfgNvjOWON64DtwaQadNnvrTAo-isE4XV47NUqtwNrsdABL0-aMiW_BMvgB3Iq08db3RmZq4RR4b7zc6OHn-1IkAZIHN0YGL0IQe3DuhN3n8qfFo07YqJ_N91nxeXn16eJDuf64ur44X5eS1otUqkpijTAiraIQ1m3bVky2siNKIoRaWFOiVaNUBxtJkcQEdbKljGDaMAWbhpwV7w6827EdtJLapSAs3wYziLDnXhj-d8aZDe_9jjNI8KLCmeDVTBD8l1HHxAcTpbZWOO3HyFndIEZh9V8gzvopqkkGvvwHeOfHkPcSOYF00UAGF1NffEDl1cUYdPdbM4J8MgW_b4pc9OLPaY8lswsy4OYAyP-dBxbH1kZy6Xs-GWnyEd8h4nAWjRGsc0eEKORKd2K0iScReP-NR3pc7z2-iazX09RsVorIL8mYi5CmgJIfPIrhKQ</recordid><startdate>20060101</startdate><enddate>20060101</enddate><creator>SU, LI-JEN</creator><creator>HSU, SHIH-LAN</creator><creator>YANG, JYH-SHYUE</creator><creator>TSENG, HUEI-HUN</creator><creator>HUANG, SHIU-FENG</creator><creator>HUANG, AND CHI-YING F.</creator><general>Cognizant Communication Corporation</general><general>Xia & He Publishing</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>7QL</scope><scope>7QO</scope><scope>7SS</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20060101</creationdate><title>Global Gene Expression Profiling of Dimethylnitrosamine-Induced Liver Fibrosis: From Pathological and Biochemical Data to Microarray Analysis</title><author>SU, LI-JEN ; HSU, SHIH-LAN ; YANG, JYH-SHYUE ; TSENG, HUEI-HUN ; HUANG, SHIU-FENG ; HUANG, AND CHI-YING F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c584t-d7c2e1213bd5008bbb76cbcf3dc111b0853ed9ddf09c51c231fcb5632596d0993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Biochemical Data</topic><topic>Biomarkers</topic><topic>Cirrhosis</topic><topic>Cluster analysis</topic><topic>Clustering</topic><topic>Dimethylnitrosamine</topic><topic>Dimethylnitrosamine - toxicity</topic><topic>Disease Models, Animal</topic><topic>DNA microarrays</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Genes</topic><topic>Genomes</topic><topic>Hepatitis</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatotoxicity</topic><topic>Histopathology</topic><topic>Liver</topic><topic>Liver - pathology</topic><topic>Liver cancer</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis - chemically induced</topic><topic>Liver Cirrhosis - genetics</topic><topic>Liver Cirrhosis - metabolism</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver diseases</topic><topic>Male</topic><topic>Microarray</topic><topic>N-Nitrosodimethylamine</topic><topic>Necroinflammatory</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Phosphatase</topic><topic>Polymerase Chain Reaction</topic><topic>Quantitative RT-PCR</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reference Values</topic><topic>Risk factors</topic><topic>Software</topic><topic>Spp1</topic><topic>Tgfb1</topic><topic>Therapeutic targets</topic><topic>Timp1</topic><topic>Transcriptomes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SU, LI-JEN</creatorcontrib><creatorcontrib>HSU, SHIH-LAN</creatorcontrib><creatorcontrib>YANG, JYH-SHYUE</creatorcontrib><creatorcontrib>TSENG, HUEI-HUN</creatorcontrib><creatorcontrib>HUANG, SHIU-FENG</creatorcontrib><creatorcontrib>HUANG, AND CHI-YING F.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>Biological Sciences</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gene expression</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SU, LI-JEN</au><au>HSU, SHIH-LAN</au><au>YANG, JYH-SHYUE</au><au>TSENG, HUEI-HUN</au><au>HUANG, SHIU-FENG</au><au>HUANG, AND CHI-YING F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Global Gene Expression Profiling of Dimethylnitrosamine-Induced Liver Fibrosis: From Pathological and Biochemical Data to Microarray Analysis</atitle><jtitle>Gene expression</jtitle><stitle>ge</stitle><addtitle>Gene Expr</addtitle><date>2006-01-01</date><risdate>2006</risdate><volume>13</volume><issue>2</issue><spage>107</spage><epage>132</epage><pages>107-132</pages><issn>1052-2166</issn><eissn>1555-3884</eissn><abstract>The development of hepatocellular carcinoma (HCC) is generally preceded by cirrhosis, which occurs at the end stage of fibrosis. This is a common and potentially lethal problem of chronic liver disease in Asia. The development of microarrays permits us to monitor transcriptomes on a
genome-wide scale; this has dramatically speeded up a comprehensive understanding of the disease process. Here we used dimethylnitrosamine (DMN), a nongenotoxic hepatotoxin, to induce rat necroinflammatory and hepatic fibrosis. During the 6-week time course, histopathological, biochemical,
and quantitative RT-PCR analyses confirmed the incidence of necroinflammatory and hepatic fibrosis in this established rat model system. Using the Affymetrix microarray chip, 256 differentially expressed genes were identified from the liver injury samples. Hierarchical clustering of gene expression
using a gene ontology database allowed the identification of several stage-specific characters and functionally related clusters that encode proteins related to metabolism, cell growth/maintenance, and response to external challenge. Among these genes, we classified 44 potential necroinflammatory-related
genes and 62 potential fibrosis-related markers or drug targets based on histopathological scores. We also compared the results with other data on well-known markers and various other microarray datasets that are available. In conclusion, we believe that the molecular picture of necroinflammatory
and hepatic fibrosis from this study may provide novel biological insights into the development of early liver damage molecular classifiers than can be used for basic research and in clinical applications. A public accessible website is available at http://LiverFibrosis.nchc.org.tw:8080/LF.</abstract><cop>Elmsford, NY</cop><pub>Cognizant Communication Corporation</pub><pmid>17017125</pmid><doi>10.3727/000000006783991872</doi><tpages>26</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies Biochemical Data Biomarkers Cirrhosis Cluster analysis Clustering Dimethylnitrosamine Dimethylnitrosamine - toxicity Disease Models, Animal DNA microarrays Fibrosis Gene expression Gene Expression Profiling Genes Genomes Hepatitis Hepatocellular carcinoma Hepatotoxicity Histopathology Liver Liver - pathology Liver cancer Liver cirrhosis Liver Cirrhosis - chemically induced Liver Cirrhosis - genetics Liver Cirrhosis - metabolism Liver Cirrhosis - pathology Liver diseases Male Microarray N-Nitrosodimethylamine Necroinflammatory Oligonucleotide Array Sequence Analysis Phosphatase Polymerase Chain Reaction Quantitative RT-PCR Rats Rats, Sprague-Dawley Reference Values Risk factors Software Spp1 Tgfb1 Therapeutic targets Timp1 Transcriptomes |
| title | Global Gene Expression Profiling of Dimethylnitrosamine-Induced Liver Fibrosis: From Pathological and Biochemical Data to Microarray Analysis |
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