ADAMs (A Disintegrin and Metalloproteinase) Messenger RNA Expression in Helicobacter pylori—Infected, Normal, and Neoplastic Gastric Mucosa
Helicobacter pylori is a risk factor for gastric cancer, and bacterial-epithelial interactions may be critical in this association. Studies using complementary DNA arrays indicated that the ADAM (A disintegrin and metalloproteinase) genes in gastric epithelial cells are differentially expressed afte...
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Veröffentlicht in: | The Journal of infectious diseases 2002-02, Vol.185 (3), p.332-340 |
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description | Helicobacter pylori is a risk factor for gastric cancer, and bacterial-epithelial interactions may be critical in this association. Studies using complementary DNA arrays indicated that the ADAM (A disintegrin and metalloproteinase) genes in gastric epithelial cells are differentially expressed after bacterial-epithelial interactions. Reverse-transcription polymerase chain reaction analysis of gastric biopsy specimens from patients with and without H. pylori showed that infection was associated with increased expression of ADAM 10 and ADAM 17 (tumor necrosis factor-α-converting enzyme) in antral mucosa, but no increases in ADAM 15 and ADAM 20 were observed. Increased ADAM 10 transcripts were observed only in cagA-negative infections. High levels of ADAM 10, ADAM 17, and ADAM 20 transcripts were present in gastric carcinoma. H. pylori stimulated temporal changes in ADAM 10 and ADAM 17 transcripts in gastric epithelial cells. Chronic infection with H. pylori may result in persistent mucosal increases in members of the ADAMs family. ADAMs-mediated ectodomain shedding may have a role in gastric carcinogenesis. |
doi_str_mv | 10.1086/338191 |
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R. ; Robinson, Philip A. ; Crabtree, Jean E.</creator><creatorcontrib>Yoshimura, Tetsuro ; Tomita, Toshihiko ; Dixon, Michael F. ; Axon, Anthony T. R. ; Robinson, Philip A. ; Crabtree, Jean E.</creatorcontrib><description>Helicobacter pylori is a risk factor for gastric cancer, and bacterial-epithelial interactions may be critical in this association. Studies using complementary DNA arrays indicated that the ADAM (A disintegrin and metalloproteinase) genes in gastric epithelial cells are differentially expressed after bacterial-epithelial interactions. Reverse-transcription polymerase chain reaction analysis of gastric biopsy specimens from patients with and without H. pylori showed that infection was associated with increased expression of ADAM 10 and ADAM 17 (tumor necrosis factor-α-converting enzyme) in antral mucosa, but no increases in ADAM 15 and ADAM 20 were observed. Increased ADAM 10 transcripts were observed only in cagA-negative infections. High levels of ADAM 10, ADAM 17, and ADAM 20 transcripts were present in gastric carcinoma. H. pylori stimulated temporal changes in ADAM 10 and ADAM 17 transcripts in gastric epithelial cells. Chronic infection with H. pylori may result in persistent mucosal increases in members of the ADAMs family. ADAMs-mediated ectodomain shedding may have a role in gastric carcinogenesis.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1573-6613</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1086/338191</identifier><identifier>PMID: 11807715</identifier><identifier>CODEN: JIDIAQ</identifier><language>eng</language><publisher>Chicago, IL: The University of Chicago Press</publisher><subject>ADAM 10 gene ; ADAM 15 gene ; ADAM 17 gene ; ADAM 20 gene ; ADAM Proteins ; ADAM10 Protein ; Adolescent ; Adult ; Aged ; Amyloid Precursor Protein Secretases ; Bacteriology ; Biological and medical sciences ; Biopsies ; Cancer ; Cell lines ; disintegrins ; Epithelial cells ; Female ; Fundamental and applied biological sciences. Psychology ; Gastric Mucosa - metabolism ; Genetics ; Glyceraldehyde-3-Phosphate Dehydrogenases - genetics ; Helicobacter Infections - metabolism ; Helicobacter pylori ; Histology ; Humans ; Infections ; Major Articles ; Male ; Membrane Proteins - genetics ; Messenger RNA ; Metalloendopeptidases - genetics ; Microbiology ; Middle Aged ; Mucosa ; RNA, Messenger - analysis ; Stomach Neoplasms - metabolism ; Tumors</subject><ispartof>The Journal of infectious diseases, 2002-02, Vol.185 (3), p.332-340</ispartof><rights>Copyright 2002 Infectious Diseases Society of America</rights><rights>2002 by the Infectious Diseases Society of America 2002</rights><rights>2002 INIST-CNRS</rights><rights>Copyright University of Chicago, acting through its Press Feb 1, 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-d3f176a5d4536a42dc9ce7bf7b9bd83e40bd7ca584848c431ee7282aa91520633</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/30137581$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/30137581$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13464145$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11807715$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yoshimura, Tetsuro</creatorcontrib><creatorcontrib>Tomita, Toshihiko</creatorcontrib><creatorcontrib>Dixon, Michael F.</creatorcontrib><creatorcontrib>Axon, Anthony T. R.</creatorcontrib><creatorcontrib>Robinson, Philip A.</creatorcontrib><creatorcontrib>Crabtree, Jean E.</creatorcontrib><title>ADAMs (A Disintegrin and Metalloproteinase) Messenger RNA Expression in Helicobacter pylori—Infected, Normal, and Neoplastic Gastric Mucosa</title><title>The Journal of infectious diseases</title><addtitle>The Journal of Infectious Diseases</addtitle><addtitle>The Journal of Infectious Diseases</addtitle><description>Helicobacter pylori is a risk factor for gastric cancer, and bacterial-epithelial interactions may be critical in this association. Studies using complementary DNA arrays indicated that the ADAM (A disintegrin and metalloproteinase) genes in gastric epithelial cells are differentially expressed after bacterial-epithelial interactions. Reverse-transcription polymerase chain reaction analysis of gastric biopsy specimens from patients with and without H. pylori showed that infection was associated with increased expression of ADAM 10 and ADAM 17 (tumor necrosis factor-α-converting enzyme) in antral mucosa, but no increases in ADAM 15 and ADAM 20 were observed. Increased ADAM 10 transcripts were observed only in cagA-negative infections. High levels of ADAM 10, ADAM 17, and ADAM 20 transcripts were present in gastric carcinoma. H. pylori stimulated temporal changes in ADAM 10 and ADAM 17 transcripts in gastric epithelial cells. Chronic infection with H. pylori may result in persistent mucosal increases in members of the ADAMs family. ADAMs-mediated ectodomain shedding may have a role in gastric carcinogenesis.</description><subject>ADAM 10 gene</subject><subject>ADAM 15 gene</subject><subject>ADAM 17 gene</subject><subject>ADAM 20 gene</subject><subject>ADAM Proteins</subject><subject>ADAM10 Protein</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Amyloid Precursor Protein Secretases</subject><subject>Bacteriology</subject><subject>Biological and medical sciences</subject><subject>Biopsies</subject><subject>Cancer</subject><subject>Cell lines</subject><subject>disintegrins</subject><subject>Epithelial cells</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastric Mucosa - metabolism</subject><subject>Genetics</subject><subject>Glyceraldehyde-3-Phosphate Dehydrogenases - genetics</subject><subject>Helicobacter Infections - metabolism</subject><subject>Helicobacter pylori</subject><subject>Histology</subject><subject>Humans</subject><subject>Infections</subject><subject>Major Articles</subject><subject>Male</subject><subject>Membrane Proteins - genetics</subject><subject>Messenger RNA</subject><subject>Metalloendopeptidases - genetics</subject><subject>Microbiology</subject><subject>Middle Aged</subject><subject>Mucosa</subject><subject>RNA, Messenger - analysis</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Tumors</subject><issn>0022-1899</issn><issn>1573-6613</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kdFqFDEYhYModq36BsooVBQ6mkwyk8zl0NZuZXeFoiDehEzmn5LtbDImM9De9QW88wl9ErPO0gVBcnHgnC_nT_gRek7we4JF8YFSQUryAM1IzmlaFIQ-RDOMsywloiwP0JMQ1hhjRgv-GB0QIjDnJJ-hn9VptQzJ2yo5NcHYAa68sYmyTbKEQXWd670bwFgV4F20QgB7BT65XFXJ2U3vo2GcTeKVOXRGu1rpIcb9bee8-X3368K2EJ3mOFk5v1Hd8d_qFbi-U2EwOjmP4qMuR-2CeooetaoL8Gynh-jrx7MvJ_N08fn84qRapJpxMaQNbQkvVN6wnBaKZY0uNfC65XVZN4ICw3XDtcoFi0czSgB4JjKlSpJnuKD0EL2ZeuPvfowQBrkxQUPXKQtuDJKIjPMciwi-_gdcu9Hb-DaZZVSUeUnEvk17F4KHVvbebJS_lQTL7XbktJ0Ivty1jfUGmj22W0cEjnaAClp1rVdWm7DnKCsYYVvu1cS5sf__sBcTsw6D8_cUxYTyXGzzdMpNGODmPlf-WhY8InL-7bucM3q5-ES5XNI_xge5ow</recordid><startdate>20020201</startdate><enddate>20020201</enddate><creator>Yoshimura, Tetsuro</creator><creator>Tomita, Toshihiko</creator><creator>Dixon, Michael F.</creator><creator>Axon, Anthony T. R.</creator><creator>Robinson, Philip A.</creator><creator>Crabtree, Jean E.</creator><general>The University of Chicago Press</general><general>University of Chicago Press</general><general>Oxford University Press</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>K9.</scope><scope>NAPCQ</scope><scope>7QL</scope><scope>C1K</scope></search><sort><creationdate>20020201</creationdate><title>ADAMs (A Disintegrin and Metalloproteinase) Messenger RNA Expression in Helicobacter pylori—Infected, Normal, and Neoplastic Gastric Mucosa</title><author>Yoshimura, Tetsuro ; Tomita, Toshihiko ; Dixon, Michael F. ; Axon, Anthony T. R. ; Robinson, Philip A. ; Crabtree, Jean E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-d3f176a5d4536a42dc9ce7bf7b9bd83e40bd7ca584848c431ee7282aa91520633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>ADAM 10 gene</topic><topic>ADAM 15 gene</topic><topic>ADAM 17 gene</topic><topic>ADAM 20 gene</topic><topic>ADAM Proteins</topic><topic>ADAM10 Protein</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Amyloid Precursor Protein Secretases</topic><topic>Bacteriology</topic><topic>Biological and medical sciences</topic><topic>Biopsies</topic><topic>Cancer</topic><topic>Cell lines</topic><topic>disintegrins</topic><topic>Epithelial cells</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gastric Mucosa - metabolism</topic><topic>Genetics</topic><topic>Glyceraldehyde-3-Phosphate Dehydrogenases - genetics</topic><topic>Helicobacter Infections - metabolism</topic><topic>Helicobacter pylori</topic><topic>Histology</topic><topic>Humans</topic><topic>Infections</topic><topic>Major Articles</topic><topic>Male</topic><topic>Membrane Proteins - genetics</topic><topic>Messenger RNA</topic><topic>Metalloendopeptidases - genetics</topic><topic>Microbiology</topic><topic>Middle Aged</topic><topic>Mucosa</topic><topic>RNA, Messenger - analysis</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoshimura, Tetsuro</creatorcontrib><creatorcontrib>Tomita, Toshihiko</creatorcontrib><creatorcontrib>Dixon, Michael F.</creatorcontrib><creatorcontrib>Axon, Anthony T. R.</creatorcontrib><creatorcontrib>Robinson, Philip A.</creatorcontrib><creatorcontrib>Crabtree, Jean E.</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yoshimura, Tetsuro</au><au>Tomita, Toshihiko</au><au>Dixon, Michael F.</au><au>Axon, Anthony T. R.</au><au>Robinson, Philip A.</au><au>Crabtree, Jean E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ADAMs (A Disintegrin and Metalloproteinase) Messenger RNA Expression in Helicobacter pylori—Infected, Normal, and Neoplastic Gastric Mucosa</atitle><jtitle>The Journal of infectious diseases</jtitle><stitle>The Journal of Infectious Diseases</stitle><addtitle>The Journal of Infectious Diseases</addtitle><date>2002-02-01</date><risdate>2002</risdate><volume>185</volume><issue>3</issue><spage>332</spage><epage>340</epage><pages>332-340</pages><issn>0022-1899</issn><eissn>1573-6613</eissn><eissn>1537-6613</eissn><coden>JIDIAQ</coden><abstract>Helicobacter pylori is a risk factor for gastric cancer, and bacterial-epithelial interactions may be critical in this association. Studies using complementary DNA arrays indicated that the ADAM (A disintegrin and metalloproteinase) genes in gastric epithelial cells are differentially expressed after bacterial-epithelial interactions. Reverse-transcription polymerase chain reaction analysis of gastric biopsy specimens from patients with and without H. pylori showed that infection was associated with increased expression of ADAM 10 and ADAM 17 (tumor necrosis factor-α-converting enzyme) in antral mucosa, but no increases in ADAM 15 and ADAM 20 were observed. Increased ADAM 10 transcripts were observed only in cagA-negative infections. High levels of ADAM 10, ADAM 17, and ADAM 20 transcripts were present in gastric carcinoma. H. pylori stimulated temporal changes in ADAM 10 and ADAM 17 transcripts in gastric epithelial cells. Chronic infection with H. pylori may result in persistent mucosal increases in members of the ADAMs family. ADAMs-mediated ectodomain shedding may have a role in gastric carcinogenesis.</abstract><cop>Chicago, IL</cop><pub>The University of Chicago Press</pub><pmid>11807715</pmid><doi>10.1086/338191</doi><tpages>9</tpages></addata></record> |
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subjects | ADAM 10 gene ADAM 15 gene ADAM 17 gene ADAM 20 gene ADAM Proteins ADAM10 Protein Adolescent Adult Aged Amyloid Precursor Protein Secretases Bacteriology Biological and medical sciences Biopsies Cancer Cell lines disintegrins Epithelial cells Female Fundamental and applied biological sciences. Psychology Gastric Mucosa - metabolism Genetics Glyceraldehyde-3-Phosphate Dehydrogenases - genetics Helicobacter Infections - metabolism Helicobacter pylori Histology Humans Infections Major Articles Male Membrane Proteins - genetics Messenger RNA Metalloendopeptidases - genetics Microbiology Middle Aged Mucosa RNA, Messenger - analysis Stomach Neoplasms - metabolism Tumors |
title | ADAMs (A Disintegrin and Metalloproteinase) Messenger RNA Expression in Helicobacter pylori—Infected, Normal, and Neoplastic Gastric Mucosa |
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