Soluble and insoluble fibronectin increase alveolar epithelial
wound healing in vitro.
Garat, Chrystelle, Farrah Kheradmand, Kurt H. Albertine, Hans G.
Folkesson, and Michael A. Matthay.
Cardiovascular Research Institute, University of California, San
Francisco, California 94143-0130, USA, Children's Research Center,
Division of Lung Biology, and Research Microscopy Facility,
University of Utah, Salt Lake City, Utah 84132-1001
APStracts 3:0124L, 1996.
Adhesive interactions between cells and extracellular matrix proteins
are important in cell attachment, migration, and proliferation. The
present work defines the role of fibronectin (soluble and insoluble)
compared to type I and type IV collagen on in vitro alveolar
epithelial wound healing. Repeated video microscopy experiments
demonstrated that the half-time of wound closure was decreased in the
presence of soluble fibronectin (6.6 +/- 2.1 hours vs. 17.4 +/- 0.8
hours in serum-free medium, P<0.05). Video microscopy, electron
microscopy and vinculin distribution demonstrated the contribution of
two main events during the repair process: the migration of
epithelial cell sheets and the spreading of the cells. During the
wound healing, the internuclear distance between two adjacent cells
at the migrating edge of the wound was significantly increased 10
hours after wounding in the presence of soluble fibronectin (67 +/-
3.0 [mu]m vs. 45 +/- 1.5 [mu]m in serum-free medium, P<0.05)
indicating that cell spreading is involved as part of the mechanism
for wound closure. Compared to type I and type IV collagen, insoluble
fibronectin was the most potent stimulus for alveolar type II cell
motility and wound healing in the absence of other serum factors.
These results demonstrate that alveolar epithelial wound healing can
be modulated in vitro by the composition of the extracellular matrix,
an effect which may be mediated by changes in cell shape.
Received 15 December 1995; accepted in final form 8 July 1996.
APS Manuscript Number L369-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 August 1996