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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