Hypoxia and reoxygenation stimulate biphasic changes in endothelial monolayer permeability.. Partridge, Catherine A. Department of Biochemistry and Molecular Biology, Albany Medical College,
APStracts 2:0032L, 1995.
Incubation of bovine pulmonary microvascular endothelial (BPMVE) cells in low O2 content (95% N2, 5% CO2) for four hours increased monolayer permeability to dextran almost two-fold, and also increased the incidence of intercellular gaps and intracellular actin stress fibers. Hypoxic incubation decreased the extracellular matrix contents of fibronectin and vitronectin, proteins which serve as anchorage points for the endothelial cells. This state was reversed after 24 hours of hypoxic incubation, and the BPMVE monolayer permeability to dextran was less than that of normoxic controls. The monolayer had fewer intercellular gaps and stress fibers, and the extracellular matrix contained increased amounts of fibronectin, vitronectin, and type I collagen. These alterations stimulated by 24 hours of hypoxic incubation were resolved within four hours of reoxygenation in room air supplemented with 5% CO2. These studies indicate that incubation of endothelial monolayers in hypoxic conditions first increases and then decreases monolayer permeability, through increased and decreased formation of intercellular gaps.

Received 17 October 1994; accepted in final form 21 February
1995.
APS Manuscript Number L295-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.