AJP - Lung Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 273: L889-L894, 1997;
1040-0605/97 $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 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 Google Scholar
Google Scholar
Right arrow Articles by Uchiba, M.
Right arrow Articles by Takatsuki, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Uchiba, M.
Right arrow Articles by Takatsuki, K.

AJP - Lung Cellular and Molecular Physiology, Vol 273, Issue 4 889-L894, Copyright © 1997 by American Physiological Society

ARTICLES

rhs-TM prevents ET-induced increase in pulmonary vascular permeability through protein C activation

M. Uchiba, K. Okajima, K. Murakami, M. Johno, M. Mohri, H. Okabe and K. Takatsuki
Department of Medicine, Kumamoto University School of Medicine, Japan.

We have previously demonstrated that recombinant human soluble (rhs) thrombomodulin (TM) inhibits the endotoxin (ET)-induced increase in pulmonary vascular permeability by inhibiting leukocyte activation. In the present study, we examined whether rhs-TM could inhibit the ET-induced increase in pulmonary vascular permeability in rats by activating protein C. rhs-TM did not inhibit ET-induced increases in pulmonary vascular permeability when its protein C activation ability was selectively inhibited by a monoclonal antibody (MAb) against rhs-TM (MAb R5G12). Histological examination revealed that neutrophil infiltration in lung tissues after ET administration was significantly reduced by rhs-TM, but infiltration was not reduced by MAb R5G12-pretreated rhs-TM. ET-induced intravascular coagulation was prevented by rhs-TM and by MAb R5G12-pretreated rhs-TM. However, ET-induced coagulation was not prevented by rhs-TM that had been treated with MAb F2H5, which cannot bind thrombin or activate protein C. These observations strongly suggest that rhs-TM prevents ET-induced pulmonary vascular injury by inhibiting pulmonary accumulation of leukocytes through thrombin binding and the subsequent protein C activation and may prevent ET-induced intravascular coagulation through thrombin binding.


This article has been cited by other articles:


Home page
 Am. J. Respir. Crit. Care Med.Home page
P. ENKHBAATAR, K. OKAJIMA, K. MURAKAMI, M. UCHIBA, H. OKABE, K. OKABE, and Y. YAMAGUCHI
Recombinant Tissue Factor Pathway Inhibitor Reduces Lipopolysaccharide-Induced Pulmonary Vascular Injury by Inhibiting Leukocyte Activation
Am. J. Respir. Crit. Care Med., November 1, 2000; 162(5): 1752 - 1759.
[Abstract] [Full Text]

Home page
 BloodHome page
F. B. Taylor Jr, D. J. Stearns-Kurosawa, S. Kurosawa, G. Ferrell, A. C. K. Chang, Z. Laszik, S. Kosanke, G. Peer, and C. T. Esmon
The endothelial cell protein C receptor aids in host defense against Escherichia coli sepsis
Blood, March 1, 2000; 95(5): 1680 - 1686.
[Abstract] [Full Text] [PDF]


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