Association of icam-1 with the cytoskeleton in rat alveolar
epithelial cells in primary culture1.
Barton, William W., Steven E. Wilcoxen, Paul J. Christensen, and
Robert Paine.
DIVISION OF PULMONARY AND CRITICAL CARE MEDICINE, DEPARTMENT OF
INTERNAL MEDICINE, UNIVERSITY OF MICHIGAN, ANN ARBOR, MICHIGAN AND
THE VETERANS ADMINISTRATION MEDICAL CENTER, ANN ARBOR MICHIGAN
APStracts 3:0103L, 1996.
Intercellular adhesion molecule-1 (ICAM-1) is a transmembrane adhesion
protein that is expressed constitutively on the apical surface of
type I cells in vivo and on type II cells in vitro as they spread in
culture assuming type I cell-like characteristics. To investigate the
possible interaction of ICAM-1 with the alveolar epithelial cell
cytoskeleton, rat type II cells in primary culture were extracted
with nonionic detergent, and residual ICAM-1 associated with the
cytoskeletal remnants was determined using immunofluorescence
microscopy, immunoprecipitation, and cell-based ELISA. A large
fraction of alveolar epithelial cell ICAM-1 remained associated with
the cytoskeleton following detergent extraction, while two other
transmembrane molecules, transferrin receptor and class II MHC, were
completely removed. ICAM-1 was redistributed on the cell surface
following the disruption of actin filaments with cytochalasin B,
suggesting interaction with the actin cytoskeleton. In contrast,
ICAM-1 was completely detergent-soluble in rat pulmonary artery
endothelial cells, human umbilical vein endothelial cells, and rat
alveolar macrophages. The association of ICAM-1 with the alveolar
epithelial cell cytoskeleton was not altered following stimulation
with inflammatory cytokines. However, detergent-resistant ICAM-1 was
significantly increased following crosslinking of ICAM-1 on the cell
surface, suggesting that this cytoskeletal association may be
modulated by interactions of alveolar epithelial cells with
inflammatory cells. The association of ICAM-1 with the cytoskeleton
in alveolar epithelial cells may provide a fixed intermediary between
mobile inflammatory cells and the alveolar surface.
Received 11 August 1995; accepted in final form 3 June 1996.
APS Manuscript Number L252-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96