AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 278: L460-L468, 2000;
1040-0605/00 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (2)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Johnson, B. A.
Right arrow Articles by Davies, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johnson, B. A.
Right arrow Articles by Davies, P.
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


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
R. Chang, L. G. Chicoine, H. Cui, N. L. Kanagy, B. R. Walker, Y. Liu, B. K. English, and L. D. Nelin
Cytokine-induced arginase activity in pulmonary endothelial cells is dependent on Src family tyrosine kinase activity
Am J Physiol Lung Cell Mol Physiol, October 1, 2008; 295(4): L688 - L697.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
J. D. Finder, J. L. Petrus, A. Hamilton, R. T. Villavicencio, B. R. Pitt, and S. M. Sebti
Signal transduction pathways of IL-1{beta}-mediated iNOS in pulmonary vascular smooth muscle cells
Am J Physiol Lung Cell Mol Physiol, October 1, 2001; 281(4): L816 - L823.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online