Fibronectin and its a5b1 integrin receptor are involved in the
wound repair process of the airway epithelium.
H[umlaut]arard, Anne-Laure, Denis Pierrot, Jocelyne Hinnrasky,
Herv[umlaut]a Kaplan, Dean Sheppard, Edith Puchelle, and Jean-Marie
Zahm.
INSERM U314, Reims, France, 2Lung Biology Center, UCSF, San
Francisco, USA
APStracts 3:0102L, 1996.
The cell migration which occurs during wound repair is dependent on
modifications of the cell-matrix interaction, in which extracellular
matrix proteins and their receptors, the integrins, are involved. In
order to study the interactions between airway epithelial cells and
the extracellular matrix during the process of wound repair, we
developed an in vitro wound model of human epithelial cells. Surface
epithelial cells were dissociated from human nasal polyps and
cultured on a type I collagen matrix. At confluency, a wound was made
by the addition of 2 ml of NaOH (1N) to the cell culture. After
washing the cell culture, the wound area was recorded every 12 hours
for 96 hours by a videomicroscopic technique. We calculated the wound
repair index representing the decrease in the wound area per hour.
Using immunofluorescence techniques, we firstly examined the
localization, during wound repair, of fibronectin and of the b1, aV,
a2, a3 and a5 integrin subunits. Secondly, we carried out a series of
wound repair blocking experiments using anti-integrin or anti
-fibronectin antibodies diluted in the culture medium. We observed
that fibronectin and the a5 integrin subunit were exclusively
expressed by the migratory cells in the wounded area. No difference
in the localization of the aV, a2, a3 integrin subunits was observed
between the non-repairing cells and the repairing cells. The blocking
experiments showed a significant decrease in the wound repair index
in the presence of either the anti-b1, anti-a3, anti-a5 or the anti
-fibronectin antibodies. Furthermore, the addition of fbronectin and
the corresponding a5b1 integrin play an important role in the process
of airway epithelium wound repair.
Received 28 December 1995; accepted in final form 10 June 1996.
APS Manuscript Number L381-5.
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