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American journal of physiology. Lung cellular and molecular physiology, 2000-07, Vol.279 (1), p.183-L193
2000
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Autor(en) / Beteiligte
Titel
Integrin alpha 3-subunit expression modulates alveolar epithelial cell monolayer formation
Ist Teil von
  • American journal of physiology. Lung cellular and molecular physiology, 2000-07, Vol.279 (1), p.183-L193
Erscheinungsjahr
2000
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
  • Division of Pulmonary and Critical Care Medicine and Will Rogers Institute Pulmonary Research Center, University of Southern California, Los Angeles, California 90033 We investigated expression of the 3 -integrin subunit by rat alveolar epithelial cells (AECs) grown in primary culture as well as the effects of monoclonal antibodies with blocking activity against the 3 -integrin subunit on AEC monolayer formation. 3 -Integrin subunit mRNA and protein were detectable in AECs on day 1  and increased with time in culture. 3 - and 1 -integrin subunits coprecipitated in immunoprecipitation experiments with 3 - and 1 -subunit-specific antibodies, consistent with their association as the 3 1 -integrin receptor at the cell membrane. Treatment with blocking anti- 3 monoclonal antibody from day 0  delayed development of transepithelial resistance, reduced transepithelial resistance through day 5  compared with that in untreated AECs, and resulted in large subconfluent patches in monolayers viewed by scanning electron microscopy on day 3.  These data indicate that 3 - and 1 -integrin subunits are expressed in AEC monolayers where they form the heterodimeric 3 1 -integrin receptor at the cell membrane. Blockade of the 3 -integrin subunit inhibits formation of confluent AEC monolayers. We conclude that the 3 -integrin subunit modulates formation of AEC monolayers by virtue of the key role of the 3 1 -integrin receptor in AEC adhesion. alveolar epithelium; 1 -integrin; cell adhesion; extracellular matrix; transepithelial resistance
Sprache
Englisch
Identifikatoren
ISSN: 1040-0605
eISSN: 1522-1504
DOI: 10.1152/ajplung.2000.279.1.L183
Titel-ID: cdi_highwire_physiology_ajplung_279_1_L183
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