AJP - Lung Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 267: L693-L703, 1994;
1040-0605/94 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 Idell, S.
Right arrow Articles by Johnson, A. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Idell, S.
Right arrow Articles by Johnson, A. R.

AJP - Lung Cellular and Molecular Physiology, Vol 267, Issue 6 693-L703, Copyright © 1994 by American Physiological Society

ARTICLES

Effects of TGF-beta and TNF-alpha on procoagulant and fibrinolytic pathways of human tracheal epithelial cells

S. Idell, A. Kumar, C. Zwieb, D. Holiday, K. B. Koenig and A. R. Johnson
Department of Medicine, University of Texas Health Science Center, Tyler 75710.

The epithelial lining of the airways is subject to injury through several processes, including infections, bronchiolitis, and fume exposures. Because airway fibrin deposition influences the course of local injury, we examined how two inflammatory cytokines influenced fibrin formation and clearance in human tracheal epithelial cells (TEC). TEC were treated with transforming growth factor-beta (TGF-beta) and tumor necrosis factor-alpha (TNF-alpha). TNF-alpha increased release of tissue factor (TF)-related procoagulant activity that, through generation of factor Xa, promotes assembly of the prothrombinase complex at the cell surface. Fibrinolytic activity was plasminogen dependent and due to both urokinase (uPA) and tissue plasminogen activator (tPA). The cells expressed plasminogen activator inhibitor 1 (PAI-1), but relatively little PAI-2. Depression of fibrinolysis by TGF-beta correlated with increased PAI-1. Conversely, TNF-alpha increased plasminogen activator (PA) activity due to increased uPA. Fibrinolytic activity was inhibited by actinomycin D and cyclohexamide, but changes in mRNAs for uPA, tPA, PAI-1, and TF by either cytokine were not appreciable. PAI-2 mRNA was not found. The data indicate that TGF-beta decreases the fibrinolytic capacity of TEC, suggesting that this cytokine promotes fibrin retention. TNF-alpha increases expression of both procoagulant and fibrinolytic activities; this differential regulation could favor both pericellular fibrin formation and dissolution.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
S. Shetty, J. Padijnayayveetil, T. Tucker, D. Stankowska, and S. Idell
The fibrinolytic system and the regulation of lung epithelial cell proteolysis, signaling, and cellular viability
Am J Physiol Lung Cell Mol Physiol, December 1, 2008; 295(6): L967 - L975.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
S. Shetty, U. R. Pendurthi, P. K. S. Halady, A. O. Azghani, and S. Idell
Urokinase induces its own expression in Beas2B lung epithelial cells
Am J Physiol Lung Cell Mol Physiol, August 1, 2002; 283(2): L319 - L328.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. Shetty and S. Idell
Urokinase Induces Expression of Its Own Receptor in Beas2B Lung Epithelial Cells
J. Biol. Chem., June 29, 2001; 276(27): 24549 - 24556.
[Abstract] [Full Text] [PDF]


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