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Am J Physiol Lung Cell Mol Physiol 278: L460-L468, 2000;
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Vol. 278, Issue 3, L460-L468, March 2000

Pulmonary arterial smooth muscle cells modulate cytokine- and LPS-induced cytotoxicity in endothelial cells

Bruce A. Johnson1, Bruce R. Pitt2, and Paul Davies3

1 Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, and 2 Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261; and 3 DuPont Pharmaceutical, Wilmington, Delaware 19880

Cytokines and lipopolysaccharide (LPS) are known to be injurious to vascular endothelial cells (ECs), but the influence of adjacent vascular smooth muscle cells (SMCs) on this injury is unknown. Exposure of cultured rat (RPMECs) or human (HPMECs) pulmonary microvascular ECs on tissue culture plastic to a mixture of cytokines (interleukin-1beta , tumor necrosis factor-alpha , and interferon-gamma ) and LPS (cytomix) resulted in a significant increase in 51Cr release to 35-40%. When unstimulated RPMECs were cocultured with cytomix-pretreated rat pulmonary microvascular SMCs (RPMSMCs) there was an increase in 51Cr release to 8.4%, which was nitric oxide dependent. However, when RPMECs or HPMECs were stimulated in direct contact with their respective SMCs, rather than a further increase in cytomix-induced injury (e.g., >35-40%), 51Cr release decreased to <10%. This cytoprotection was fully reproduced with fixed RPMSMCs, and partially reproduced by plating HPMECs on gelatin. These data show that the direct toxicity of a cytokine and endotoxin mixture on cultured ECs can be reduced by contact with vascular smooth muscle.

pulmonary microcirculation; pulmonary endothelium; pulmonary vascular smooth muscle; nitric oxide; human; rat; cytokines; endotoxin; lipopolysaccharide


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