Mucin gene expression in rat airways following infection and irritation
Identifieur interne : 000133 ( Istex/Curation ); précédent : 000132; suivant : 000134Mucin gene expression in rat airways following infection and irritation
Auteurs : Berthold Jany [Allemagne] ; Marianne Gallup [États-Unis] ; Tohru Tsuda [États-Unis] ; Carol Basbaum [États-Unis]Source :
- 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
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Würzburg</wicri:regionArea></affiliation></author><author><name sortKey="Gallup, Marianne" sort="Gallup, Marianne" uniqKey="Gallup M" first="Marianne" last="Gallup">Marianne Gallup</name><affiliation wicri:level="1"><mods:affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143</wicri:regionArea></affiliation></author><author><name sortKey="Tsuda, Tohru" sort="Tsuda, Tohru" uniqKey="Tsuda T" first="Tohru" last="Tsuda">Tohru Tsuda</name><affiliation wicri:level="1"><mods:affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143</wicri:regionArea></affiliation></author><author><name sortKey="Basbaum, Carol" sort="Basbaum, Carol" uniqKey="Basbaum C" first="Carol" last="Basbaum">Carol Basbaum</name><affiliation wicri:level="1"><mods:affiliation>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Anatomy and Cardiovascular, Research Institute, University of California, San Francisco, San Francisco, California 94143</wicri:regionArea></affiliation><affiliation wicri:level="2"><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><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>To whom correspondence should be addressed at Department of Anatomy & CVRI, Box 0130, HSE 1331, 513 Parnassus, San Francisco</wicri:cityArea></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. These results suggest that pathogen-and irritant-induced hypersecretion may be partly controlled at the level of mucin mRNA.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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