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Insights into psoriasis and other inflammatory diseases from large-scale gene expression studies
Approximately 2% of the Caucasian population is affected by psoriasis (PS); a chronic inflammatory skin disease triggered by both genetic and environmental risk factors. In addition to a major contribution from the HLA class I region, PS susceptibility loci have been mapped to a number of regions in...
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Published in: | Human molecular genetics 2001-08, Vol.10 (17), p.1793-1805 |
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description | Approximately 2% of the Caucasian population is affected by psoriasis (PS); a chronic inflammatory skin disease triggered by both genetic and environmental risk factors. In addition to a major contribution from the HLA class I region, PS susceptibility loci have been mapped to a number of regions including 1q21, 3q21, 4qter, 14q31-q32, 17q24-q25, 19p13.3 and 20p. Some of these overlap with loci implicated in other autoimmune/inflammatory diseases. Global gene expression studies are beginning to provide insights into the etiology of these and other complex diseases. We used Affymetrix oligonucleotide arrays comprising approximately 12 000 known genes to initiate a more comprehensive analysis of the transcriptional changes that occur in involved and uninvolved skin of 15 psoriatic patients versus six normal controls. Expression levels of the transcripts detected on the arrays were first used to determine the relationship of samples to each other using hierarchical clustering. This analysis clearly differentiated involved psoriatic skin from uninvolved and normal skin. Clusters of differentially expressed genes with similar expression patterns in the same samples were then identified. Six out of 32 clusters contained a total of 177 transcripts that were differentially expressed in involved psoriatic skin versus normal skin. These differences were independent of the gender, age, skin site and HLA class I status of the patient. Ten of the 177 genes were also differentially expressed in uninvolved skin, and several mapped to regions previously shown to harbor psoriasis susceptibility loci. |
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In addition to a major contribution from the HLA class I region, PS susceptibility loci have been mapped to a number of regions including 1q21, 3q21, 4qter, 14q31-q32, 17q24-q25, 19p13.3 and 20p. Some of these overlap with loci implicated in other autoimmune/inflammatory diseases. Global gene expression studies are beginning to provide insights into the etiology of these and other complex diseases. We used Affymetrix oligonucleotide arrays comprising approximately 12 000 known genes to initiate a more comprehensive analysis of the transcriptional changes that occur in involved and uninvolved skin of 15 psoriatic patients versus six normal controls. Expression levels of the transcripts detected on the arrays were first used to determine the relationship of samples to each other using hierarchical clustering. This analysis clearly differentiated involved psoriatic skin from uninvolved and normal skin. Clusters of differentially expressed genes with similar expression patterns in the same samples were then identified. Six out of 32 clusters contained a total of 177 transcripts that were differentially expressed in involved psoriatic skin versus normal skin. These differences were independent of the gender, age, skin site and HLA class I status of the patient. Ten of the 177 genes were also differentially expressed in uninvolved skin, and several mapped to regions previously shown to harbor psoriasis susceptibility loci.</description><identifier>ISSN: 0964-6906</identifier><identifier>ISSN: 1460-2083</identifier><identifier>EISSN: 1460-2083</identifier><identifier>DOI: 10.1093/hmg/10.17.1793</identifier><identifier>PMID: 11532989</identifier><identifier>CODEN: HNGEE5</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Autoimmune Diseases - genetics ; Biological and medical sciences ; chromosome 1 ; chromosome 14 ; chromosome 17 ; chromosome 19 ; chromosome 20 ; chromosome 3 ; chromosome 4 ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation ; Genes, MHC Class I ; Genetic Predisposition to Disease ; Glycoproteins - genetics ; Humans ; Male ; Molecular and cellular biology ; Multigene Family ; Oligonucleotide Array Sequence Analysis - methods ; Phylogeny ; Proteins - genetics ; Psoriasis - etiology ; Psoriasis - genetics ; RNA, Messenger - metabolism ; Skin - metabolism ; Transcription, Genetic</subject><ispartof>Human molecular genetics, 2001-08, Vol.10 (17), p.1793-1805</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Aug 15, 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-1011ad6957f3c5079e401a5890c963b1317933cbd07843d534cd89ba29a2ebb73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14159680$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11532989$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BOWCOCK, Anne M</creatorcontrib><creatorcontrib>SHANNON, William</creatorcontrib><creatorcontrib>FENGHE DU</creatorcontrib><creatorcontrib>DUNCAN, Jill</creatorcontrib><creatorcontrib>KAI CAO</creatorcontrib><creatorcontrib>AFTERGUT, Kent</creatorcontrib><creatorcontrib>CATIER, Jennifer</creatorcontrib><creatorcontrib>FERNANDEZ-VINA, Marcelo A</creatorcontrib><creatorcontrib>MENTER, Alan</creatorcontrib><title>Insights into psoriasis and other inflammatory diseases from large-scale gene expression studies</title><title>Human molecular genetics</title><addtitle>Hum Mol Genet</addtitle><description>Approximately 2% of the Caucasian population is affected by psoriasis (PS); a chronic inflammatory skin disease triggered by both genetic and environmental risk factors. In addition to a major contribution from the HLA class I region, PS susceptibility loci have been mapped to a number of regions including 1q21, 3q21, 4qter, 14q31-q32, 17q24-q25, 19p13.3 and 20p. Some of these overlap with loci implicated in other autoimmune/inflammatory diseases. Global gene expression studies are beginning to provide insights into the etiology of these and other complex diseases. We used Affymetrix oligonucleotide arrays comprising approximately 12 000 known genes to initiate a more comprehensive analysis of the transcriptional changes that occur in involved and uninvolved skin of 15 psoriatic patients versus six normal controls. Expression levels of the transcripts detected on the arrays were first used to determine the relationship of samples to each other using hierarchical clustering. This analysis clearly differentiated involved psoriatic skin from uninvolved and normal skin. Clusters of differentially expressed genes with similar expression patterns in the same samples were then identified. Six out of 32 clusters contained a total of 177 transcripts that were differentially expressed in involved psoriatic skin versus normal skin. These differences were independent of the gender, age, skin site and HLA class I status of the patient. Ten of the 177 genes were also differentially expressed in uninvolved skin, and several mapped to regions previously shown to harbor psoriasis susceptibility loci.</description><subject>Autoimmune Diseases - genetics</subject><subject>Biological and medical sciences</subject><subject>chromosome 1</subject><subject>chromosome 14</subject><subject>chromosome 17</subject><subject>chromosome 19</subject><subject>chromosome 20</subject><subject>chromosome 3</subject><subject>chromosome 4</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation</subject><subject>Genes, MHC Class I</subject><subject>Genetic Predisposition to Disease</subject><subject>Glycoproteins - genetics</subject><subject>Humans</subject><subject>Male</subject><subject>Molecular and cellular biology</subject><subject>Multigene Family</subject><subject>Oligonucleotide Array Sequence Analysis - methods</subject><subject>Phylogeny</subject><subject>Proteins - genetics</subject><subject>Psoriasis - etiology</subject><subject>Psoriasis - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Skin - metabolism</subject><subject>Transcription, Genetic</subject><issn>0964-6906</issn><issn>1460-2083</issn><issn>1460-2083</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNqF0UFr3DAQBWBRWprtttceiyikNycaS5Y8xxKaNhDoJTm7sjzeVbCtrcaG5t_XmywEeikINKCPgacnxEdQF6BQX-7H3eVxdutB_UpswFhVlKrWr8VGoTWFRWXPxDvmB6XAGu3eijOASpdY40b8upk47vYzyzjNSR445eg5svRTJ9O8p7w-9IMfRz-n_Ci7yOSZWPY5jXLweUcFBz-Q3NFEkv4cMjHHNEmely4Svxdvej8wfTjdW3F__e3u6kdx-_P7zdXX2yIYwLkABeA7i5XrdaiUQzIKfFWjCmh1C_oYT4e2U642uqu0CV2NrS_Rl9S2Tm_Fl-e9h5x-L8RzM0YONAx-orRw4wA0Gqf_C6FepUOzws__wIe05GkN0ZQApbIacEUXzyjkxJypbw45jj4_NqCaY0PN2tDT7JqnCFvx6bR1aUfqXvipkhWcn4A_fmyf_RQivzgDFdpa6b8PDpkY</recordid><startdate>20010815</startdate><enddate>20010815</enddate><creator>BOWCOCK, Anne M</creator><creator>SHANNON, William</creator><creator>FENGHE DU</creator><creator>DUNCAN, Jill</creator><creator>KAI CAO</creator><creator>AFTERGUT, Kent</creator><creator>CATIER, Jennifer</creator><creator>FERNANDEZ-VINA, Marcelo A</creator><creator>MENTER, Alan</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</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>7QP</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20010815</creationdate><title>Insights into psoriasis and other inflammatory diseases from large-scale gene expression studies</title><author>BOWCOCK, Anne M ; SHANNON, William ; FENGHE DU ; DUNCAN, Jill ; KAI CAO ; AFTERGUT, Kent ; CATIER, Jennifer ; FERNANDEZ-VINA, Marcelo A ; MENTER, Alan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-1011ad6957f3c5079e401a5890c963b1317933cbd07843d534cd89ba29a2ebb73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Autoimmune Diseases - genetics</topic><topic>Biological and medical sciences</topic><topic>chromosome 1</topic><topic>chromosome 14</topic><topic>chromosome 17</topic><topic>chromosome 19</topic><topic>chromosome 20</topic><topic>chromosome 3</topic><topic>chromosome 4</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation</topic><topic>Genes, MHC Class I</topic><topic>Genetic Predisposition to Disease</topic><topic>Glycoproteins - genetics</topic><topic>Humans</topic><topic>Male</topic><topic>Molecular and cellular biology</topic><topic>Multigene Family</topic><topic>Oligonucleotide Array Sequence Analysis - methods</topic><topic>Phylogeny</topic><topic>Proteins - genetics</topic><topic>Psoriasis - etiology</topic><topic>Psoriasis - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Skin - metabolism</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BOWCOCK, Anne M</creatorcontrib><creatorcontrib>SHANNON, William</creatorcontrib><creatorcontrib>FENGHE DU</creatorcontrib><creatorcontrib>DUNCAN, Jill</creatorcontrib><creatorcontrib>KAI CAO</creatorcontrib><creatorcontrib>AFTERGUT, Kent</creatorcontrib><creatorcontrib>CATIER, Jennifer</creatorcontrib><creatorcontrib>FERNANDEZ-VINA, Marcelo A</creatorcontrib><creatorcontrib>MENTER, Alan</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Human molecular genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BOWCOCK, Anne M</au><au>SHANNON, William</au><au>FENGHE DU</au><au>DUNCAN, Jill</au><au>KAI CAO</au><au>AFTERGUT, Kent</au><au>CATIER, Jennifer</au><au>FERNANDEZ-VINA, Marcelo A</au><au>MENTER, Alan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Insights into psoriasis and other inflammatory diseases from large-scale gene expression studies</atitle><jtitle>Human molecular genetics</jtitle><addtitle>Hum Mol Genet</addtitle><date>2001-08-15</date><risdate>2001</risdate><volume>10</volume><issue>17</issue><spage>1793</spage><epage>1805</epage><pages>1793-1805</pages><issn>0964-6906</issn><issn>1460-2083</issn><eissn>1460-2083</eissn><coden>HNGEE5</coden><abstract>Approximately 2% of the Caucasian population is affected by psoriasis (PS); a chronic inflammatory skin disease triggered by both genetic and environmental risk factors. In addition to a major contribution from the HLA class I region, PS susceptibility loci have been mapped to a number of regions including 1q21, 3q21, 4qter, 14q31-q32, 17q24-q25, 19p13.3 and 20p. Some of these overlap with loci implicated in other autoimmune/inflammatory diseases. Global gene expression studies are beginning to provide insights into the etiology of these and other complex diseases. We used Affymetrix oligonucleotide arrays comprising approximately 12 000 known genes to initiate a more comprehensive analysis of the transcriptional changes that occur in involved and uninvolved skin of 15 psoriatic patients versus six normal controls. Expression levels of the transcripts detected on the arrays were first used to determine the relationship of samples to each other using hierarchical clustering. This analysis clearly differentiated involved psoriatic skin from uninvolved and normal skin. Clusters of differentially expressed genes with similar expression patterns in the same samples were then identified. Six out of 32 clusters contained a total of 177 transcripts that were differentially expressed in involved psoriatic skin versus normal skin. These differences were independent of the gender, age, skin site and HLA class I status of the patient. Ten of the 177 genes were also differentially expressed in uninvolved skin, and several mapped to regions previously shown to harbor psoriasis susceptibility loci.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>11532989</pmid><doi>10.1093/hmg/10.17.1793</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Autoimmune Diseases - genetics Biological and medical sciences chromosome 1 chromosome 14 chromosome 17 chromosome 19 chromosome 20 chromosome 3 chromosome 4 Female Fundamental and applied biological sciences. Psychology Gene Expression Regulation Genes, MHC Class I Genetic Predisposition to Disease Glycoproteins - genetics Humans Male Molecular and cellular biology Multigene Family Oligonucleotide Array Sequence Analysis - methods Phylogeny Proteins - genetics Psoriasis - etiology Psoriasis - genetics RNA, Messenger - metabolism Skin - metabolism Transcription, Genetic |
title | Insights into psoriasis and other inflammatory diseases from large-scale gene expression studies |
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