Mucin gene expression in rat airways following infection and irritation
Identifieur interne : 000153 ( Istex/Corpus ); précédent : 000152; suivant : 000154Mucin gene expression in rat airways following infection and irritation
Auteurs : Berthold Jany ; Marianne Gallup ; Tohru Tsuda ; Carol BasbaumSource :
- Biochemical and Biophysical Research Communications [ 0006-291X ] ; 1991.
English descriptors
- Teeft :
- Airway, Airway epithelial cells, Airway mucin mrna, Animal colony, Biophysical, Biophysical research communications, Bronchial epithelium, Bronchitis, Cdna, Chronic bronchitis, Control rats, Corona virus, Cystic fibrosis, Degradation rate, Electron microscopy, Glycoprotein, Healthy dogs, High abundance, Human intestine, Hybridization, Hybridized, Intestine, Lower panel, Major mucus glycoprotein, Mrna, Mucin, Mucin cdna smuc, Mucin cdnas, Mucin edna, Mucin gene expression, Mucin hybridization signals, Mucin mrna, Mucin mrna induction, Mucous, Mucous cells, Mucus, Mucus glycoproteins, Mucus hypersecretion, Northern blots, Pathogen, Rat, Respiratory tract infections, Sendai, Sendai rats, Sendai virus, Sendal virus, Significant antibody titer, Significant antibody titers, Smuc, Sodium chloride, Sodium citrate, Specific mrnas, Specific rats, Upper panel, Uranyl acetate.
Abstract
Summary: Airway mucus hypersecretion occurs in response to infection and irritation and poses an important and poorly understood clinical problem. In order to gain insight into its pathogenesis, we have focused on an mRNA encoding the major mucus glycoprotein, mucin. Northern blots showed that mucin mRNA was abundant in the intestine of specific pathogen free rats whereas it was undetectable in the airways of these rats until pathogen-free conditions were suspended and rats acquired Sendai (Parainfluenza I) virus infections. Airway mucin hybridization signals in rats that were both infected with Sendai virus and exposed to SO2were more intense than those in rats with infection alone. These results suggest that pathogen-and irritant-induced hypersecretion may be partly controlled at the level of mucin mRNA.
Url:
DOI: 10.1016/S0006-291X(05)81373-7
Links to Exploration step
ISTEX:251BB4FDFF6773FE8053EA2A410A967EEF59634ELe document en format XML
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USA</mods:affiliation></affiliation></author><author><name sortKey="Tsuda, Tohru" sort="Tsuda, Tohru" uniqKey="Tsuda T" first="Tohru" last="Tsuda">Tohru Tsuda</name><affiliation><mods:affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</mods:affiliation></affiliation></author><author><name sortKey="Basbaum, Carol" sort="Basbaum, Carol" uniqKey="Basbaum C" first="Carol" last="Basbaum">Carol Basbaum</name><affiliation><mods:affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>To whom correspondence should be addressed at Department of Anatomy & CVRI, Box 0130, HSE 1331, 513 Parnassus, San Francisco, CA 94143.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Biochemical and Biophysical Research Communications</title><title level="j" type="abbrev">YBBRC</title><idno type="ISSN">0006-291X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">181</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="1">1</biblScope><biblScope unit="page" to="8">8</biblScope></imprint><idno type="ISSN">0006-291X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-291X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Airway</term><term>Airway epithelial cells</term><term>Airway mucin mrna</term><term>Animal colony</term><term>Biophysical</term><term>Biophysical research communications</term><term>Bronchial epithelium</term><term>Bronchitis</term><term>Cdna</term><term>Chronic bronchitis</term><term>Control rats</term><term>Corona virus</term><term>Cystic fibrosis</term><term>Degradation rate</term><term>Electron microscopy</term><term>Glycoprotein</term><term>Healthy dogs</term><term>High abundance</term><term>Human intestine</term><term>Hybridization</term><term>Hybridized</term><term>Intestine</term><term>Lower panel</term><term>Major mucus glycoprotein</term><term>Mrna</term><term>Mucin</term><term>Mucin cdna smuc</term><term>Mucin cdnas</term><term>Mucin edna</term><term>Mucin gene expression</term><term>Mucin hybridization signals</term><term>Mucin mrna</term><term>Mucin mrna induction</term><term>Mucous</term><term>Mucous cells</term><term>Mucus</term><term>Mucus glycoproteins</term><term>Mucus hypersecretion</term><term>Northern blots</term><term>Pathogen</term><term>Rat</term><term>Respiratory tract infections</term><term>Sendai</term><term>Sendai rats</term><term>Sendai virus</term><term>Sendal virus</term><term>Significant antibody titer</term><term>Significant antibody titers</term><term>Smuc</term><term>Sodium chloride</term><term>Sodium citrate</term><term>Specific mrnas</term><term>Specific rats</term><term>Upper panel</term><term>Uranyl acetate</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Airway mucus hypersecretion occurs in response to infection and irritation and poses an important and poorly understood clinical problem. In order to gain insight into its pathogenesis, we have focused on an mRNA encoding the major mucus glycoprotein, mucin. Northern blots showed that mucin mRNA was abundant in the intestine of specific pathogen free rats whereas it was undetectable in the airways of these rats until pathogen-free conditions were suspended and rats acquired Sendai (Parainfluenza I) virus infections. Airway mucin hybridization signals in rats that were both infected with Sendai virus and exposed to SO2were more intense than those in rats with infection alone. 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In order to gain insight into its pathogenesis, we have focused on an mRNA encoding the major mucus glycoprotein, mucin. Northern blots showed that mucin mRNA was abundant in the intestine of specific pathogen free rats whereas it was undetectable in the airways of these rats until pathogen-free conditions were suspended and rats acquired Sendai (Parainfluenza I) virus infections. Airway mucin hybridization signals in rats that were both infected with Sendai virus and exposed to SO2were more intense than those in rats with infection alone. These results suggest that pathogen-and irritant-induced hypersecretion may be partly controlled at the level of mucin mRNA.</abstract><qualityIndicators><score>6.881</score><pdfWordCount>3417</pdfWordCount><pdfCharCount>20501</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>122</abstractWordCount><abstractCharCount>817</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Mucin gene expression in rat airways following infection and irritation</title><pmid><json:string>1659805</json:string></pmid><pii><json:string>S0006-291X(05)81373-7</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Natl. Acad. Sci. 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science</json:string><json:string>2 - biophysics</json:string><json:string>2 - biochemistry & molecular biology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - biochemistry & molecular biology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cell Biology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Molecular Biology</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Biochemistry</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Biophysics</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1991</publicationDate><copyrightDate>1991</copyrightDate><doi><json:string>10.1016/S0006-291X(05)81373-7</json:string></doi><id>251BB4FDFF6773FE8053EA2A410A967EEF59634E</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-Z5R556CJ-T/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-Z5R556CJ-T/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-Z5R556CJ-T/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Mucin gene expression in rat airways following infection and irritation</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©1991 Academic Press, Inc.</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>1991</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Mucin gene expression in rat airways following infection and irritation</title><author xml:id="author-0000"><persName><forename type="first">Berthold</forename><surname>Jany</surname></persName><affiliation>Medizin Poliklinik der Universitat, Klinikstrasse 6-8, D-8700 Würzburg, Germany</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Marianne</forename><surname>Gallup</surname></persName><affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Tohru</forename><surname>Tsuda</surname></persName><affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Carol</forename><surname>Basbaum</surname></persName><affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</affiliation><affiliation>To whom correspondence should be addressed at Department of Anatomy & CVRI, Box 0130, HSE 1331, 513 Parnassus, San Francisco, CA 94143.</affiliation></author><idno type="istex">251BB4FDFF6773FE8053EA2A410A967EEF59634E</idno><idno type="ark">ark:/67375/6H6-Z5R556CJ-T</idno><idno type="DOI">10.1016/S0006-291X(05)81373-7</idno><idno type="PII">S0006-291X(05)81373-7</idno><idno type="article-id">5813737</idno></analytic><monogr><title level="j">Biochemical and Biophysical Research Communications</title><title level="j" type="abbrev">YBBRC</title><idno type="pISSN">0006-291X</idno><idno type="PII">S0006-291X(05)X1372-9</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991"></date><biblScope unit="volume">181</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="1">1</biblScope><biblScope unit="page" to="8">8</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1991</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: Airway mucus hypersecretion occurs in response to infection and irritation and poses an important and poorly understood clinical problem. In order to gain insight into its pathogenesis, we have focused on an mRNA encoding the major mucus glycoprotein, mucin. Northern blots showed that mucin mRNA was abundant in the intestine of specific pathogen free rats whereas it was undetectable in the airways of these rats until pathogen-free conditions were suspended and rats acquired Sendai (Parainfluenza I) virus infections. Airway mucin hybridization signals in rats that were both infected with Sendai virus and exposed to SO2were more intense than those in rats with infection alone. These results suggest that pathogen-and irritant-induced hypersecretion may be partly controlled at the level of mucin mRNA.</p></abstract></profileDesc><revisionDesc><change when="1991">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-Z5R556CJ-T/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier doc found" wicri:toSee="Elsevier, no converted or simple article"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 5.0.1//EN//XML" URI="art501.dtd" name="istex:docType"></istex:docType><istex:document><article version="5.0" xml:lang="en" docsubtype="fla"><item-info><jid>YBBRC</jid><aid>5813737</aid><ce:pii>S0006-291X(05)81373-7</ce:pii><ce:doi>10.1016/S0006-291X(05)81373-7</ce:doi><ce:copyright type="unknown" year="1991">Academic Press, Inc.</ce:copyright></item-info><head><ce:title>Mucin gene expression in rat airways following infection and irritation</ce:title><ce:author-group><ce:author><ce:given-name>Berthold</ce:given-name><ce:surname>Jany</ce:surname><ce:cross-ref refid="aff1"><ce:sup loc="post">†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Marianne</ce:given-name><ce:surname>Gallup</ce:surname><ce:cross-ref refid="aff2"><ce:sup loc="post">§</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Tohru</ce:given-name><ce:surname>Tsuda</ce:surname><ce:cross-ref refid="aff2"><ce:sup loc="post">§</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Carol</ce:given-name><ce:surname>Basbaum</ce:surname><ce:cross-ref refid="aff2"><ce:sup loc="post">§</ce:sup></ce:cross-ref><ce:cross-ref refid="cor1"><ce:sup loc="post">*</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="aff1"><ce:label>†</ce:label><ce:textfn>Medizin Poliklinik der Universitat, Klinikstrasse 6-8, D-8700 Würzburg, Germany</ce:textfn></ce:affiliation><ce:affiliation id="aff2"><ce:label>§</ce:label><ce:textfn>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</ce:textfn></ce:affiliation><ce:correspondence id="cor1"><ce:label>*</ce:label><ce:text>To whom correspondence should be addressed at Department of Anatomy & CVRI, Box 0130, HSE 1331, 513 Parnassus, San Francisco, CA 94143.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="30" month="9" year="1991"></ce:date-received><ce:abstract id="ab1" class="author" xml:lang="en"><ce:section-title>Summary</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">Airway mucus hypersecretion occurs in response to infection and irritation and poses an important and poorly understood clinical problem. In order to gain insight into its pathogenesis, we have focused on an mRNA encoding the major mucus glycoprotein, mucin. Northern blots showed that mucin mRNA was abundant in the intestine of specific pathogen free rats whereas it was undetectable in the airways of these rats until pathogen-free conditions were suspended and rats acquired Sendai (Parainfluenza I) virus infections. Airway mucin hybridization signals in rats that were both infected with Sendai virus and exposed to SO<ce:inf loc="post">2</ce:inf>were more intense than those in rats with infection alone. These results suggest that pathogen-and irritant-induced hypersecretion may be partly controlled at the level of mucin mRNA.</ce:simple-para></ce:abstract-sec></ce:abstract></head><tail view="all"><ce:bibliography view="all" id="bibliography.0010"><ce:section-title>References</ce:section-title><ce:bibliography-sec id="bibliography-sec.0010"><ce:bib-reference id="bib1"><ce:label>[1]</ce:label><sb:reference><sb:contribution langtype="en"><sb:authors><sb:author><ce:surname>A.T.S.</ce:surname></sb:author></sb:authors><sb:title><sb:maintitle>Chronic bronchitis, asthma, and pulmonary emphysema</sb:maintitle></sb:title></sb:contribution><sb:host><sb:issue><sb:series><sb:title><sb:maintitle>Am. Rev. Respir. 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Physiol.</sb:maintitle></sb:title><sb:volume-nr>259</sb:volume-nr></sb:series><sb:date>1990</sb:date></sb:issue><sb:pages><sb:first-page>L38</sb:first-page><sb:last-page>L46</sb:last-page></sb:pages></sb:host></sb:reference></ce:bib-reference></ce:bibliography-sec></ce:bibliography></tail></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Mucin gene expression in rat airways following infection and irritation</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Mucin gene expression in rat airways following infection and irritation</title></titleInfo><name type="personal"><namePart type="given">Berthold</namePart><namePart type="family">Jany</namePart><affiliation>Medizin Poliklinik der Universitat, Klinikstrasse 6-8, D-8700 Würzburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marianne</namePart><namePart type="family">Gallup</namePart><affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tohru</namePart><namePart type="family">Tsuda</namePart><affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carol</namePart><namePart type="family">Basbaum</namePart><affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</affiliation><affiliation>To whom correspondence should be addressed at Department of Anatomy & CVRI, Box 0130, HSE 1331, 513 Parnassus, San Francisco, CA 94143.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1991</dateIssued><copyrightDate encoding="w3cdtf">1991</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Summary: Airway mucus hypersecretion occurs in response to infection and irritation and poses an important and poorly understood clinical problem. In order to gain insight into its pathogenesis, we have focused on an mRNA encoding the major mucus glycoprotein, mucin. Northern blots showed that mucin mRNA was abundant in the intestine of specific pathogen free rats whereas it was undetectable in the airways of these rats until pathogen-free conditions were suspended and rats acquired Sendai (Parainfluenza I) virus infections. Airway mucin hybridization signals in rats that were both infected with Sendai virus and exposed to SO2were more intense than those in rats with infection alone. These results suggest that pathogen-and irritant-induced hypersecretion may be partly controlled at the level of mucin mRNA.</abstract><relatedItem type="host"><titleInfo><title>Biochemical and Biophysical Research Communications</title></titleInfo><titleInfo type="abbreviated"><title>YBBRC</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1991</dateIssued></originInfo><identifier type="ISSN">0006-291X</identifier><identifier type="PII">S0006-291X(05)X1372-9</identifier><part><date>1991</date><detail type="volume"><number>181</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>505</end></extent><extent unit="pages"><start>1</start><end>8</end></extent></part></relatedItem><identifier type="istex">251BB4FDFF6773FE8053EA2A410A967EEF59634E</identifier><identifier type="ark">ark:/67375/6H6-Z5R556CJ-T</identifier><identifier type="DOI">10.1016/S0006-291X(05)81373-7</identifier><identifier type="PII">S0006-291X(05)81373-7</identifier><identifier type="ArticleID">5813737</identifier><accessCondition type="use and reproduction" contentType="copyright">©1991 Academic Press, Inc.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Academic Press, Inc., ©1991</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-Z5R556CJ-T/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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