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Am J Physiol Lung Cell Mol Physiol 279: L183-L193, 2000;
1040-0605/00 $5.00
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Vol. 279, Issue 1, L183-L193, July 2000

Integrin alpha 3-subunit expression modulates alveolar epithelial cell monolayer formation

Richard L. Lubman, Xiao-Ling Zhang, Jie Zheng, Leah Ocampo, Melissa Z. Lopez, Srihari Veeraraghavan, Stephanie M. Zabski, Spencer I. Danto, and Zea Borok

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 alpha 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 alpha 3-integrin subunit on AEC monolayer formation. alpha 3-Integrin subunit mRNA and protein were detectable in AECs on day 1 and increased with time in culture. alpha 3- and beta 1-integrin subunits coprecipitated in immunoprecipitation experiments with alpha 3- and beta 1-subunit-specific antibodies, consistent with their association as the alpha 3beta 1-integrin receptor at the cell membrane. Treatment with blocking anti-alpha 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 alpha 3- and beta 1-integrin subunits are expressed in AEC monolayers where they form the heterodimeric alpha 3beta 1-integrin receptor at the cell membrane. Blockade of the alpha 3-integrin subunit inhibits formation of confluent AEC monolayers. We conclude that the alpha 3-integrin subunit modulates formation of AEC monolayers by virtue of the key role of the alpha 3beta 1-integrin receptor in AEC adhesion.

alveolar epithelium; beta 1-integrin; cell adhesion; extracellular matrix; transepithelial resistance


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