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.