AJP - Lung Columbus Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol (July 26, 2002). doi:10.1152/ajplung.00231.2001
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/6/L1239    most recent
00231.2001v1
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 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 Web of Science (11)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lahiri, T.
Right arrow Articles by Shore, S. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lahiri, T.
Right arrow Articles by Shore, S. A.

Articles in PresS, published online ahead of print July 26, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00231.2001
Submitted on June 18, 2001
Accepted on July 22, 2002

THE EFFECT OF IL-1ß ON CRE DEPENDENT GENE EXPRESSION IN HUMAN AIRWAY SMOOTH MUSCLE CELLS

Thomas Lahiri1, Paul E. Moore1, Simonetta Baraldo1, Timothy R. Whitehead1, Matthew D. McKenna1, Reynold A. Panettieri, Jr.2, and Stephanie A. Shore1*

1 Physiology Program, Harvard School of Public Health, Boston, MA, USA
2 Pulmonary and Critical Care Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA

* To whom correspondence should be addressed. E-mail: sshore{at}hsph.harvard.edu.

IL-1ß inhibits isoproterenol (ISO) induced relaxation of cultured human airway smooth muscle (HASM) cells. The purpose of this study was to determine whether IL-1ß can also suppress ISO-induced cAMP response element (CRE) dependent gene expression. ISO (10 µM) caused a marked increase in CRE-binding protein (CREB) phosphorylation which was attenuated by IL-1ß(2ng/ml). This effect of IL-1ß was abolished by the COX inhibitor indomethacin. To examine CRE driven gene expression, we transiently transfected HASM cells with a construct containing CRE elements upstream of a luciferase reporter gene. ISO (6h) caused a 6-fold increase in luciferase activity. IL-1ß(24h) alone also increased luciferase activity, though to a lesser extent (2-fold). However the ability of ISO to elicit luciferase expression was marked reduced in cells treated with IL-1ß. The MEK and p38 inhibitors, U0126 and SB203580, the COX inhibitor indomethacin, the PKA inhibitor H-89, and the glucocorticoid dexamethasone, each completely abolished the ability of IL-1ß to induce CRE driven gene expression, but only slightly increased the ability of ISO to induce CRE driven gene expression in IL-1ß treated cells. IL-1ß also attenuated db cAMP induced CRE driven gene expression, but not db cAMP induced CREB phosphorylation. TNF{alpha}(10 ng/ml) also attenuated ISO-induced CRE driven gene expression, even though it was without effect on ISO-induced cAMP formation or ISO-induced CREB phosphorylation. The results suggest that IL-1ß and TNF{alpha}may attenuate the ability of ß-agonists to induce expression of genes with CRE elements in their regulatory regions, through events downstream of PKA.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
A. M. Goldsmith, M. B. Hershenson, M. P. Wolbert, and J. K. Bentley
Regulation of airway smooth muscle {alpha}-actin expression by glucocorticoids
Am J Physiol Lung Cell Mol Physiol, January 1, 2007; 292(1): L99 - L106.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
D. S. Faffe, L. Flynt, M. Mellema, T. R. Whitehead, K. Bourgeois, R. A. Panettieri Jr., E. S. Silverman, and S. A. Shore
Oncostatin M causes VEGF release from human airway smooth muscle: synergy with IL-1{beta}
Am J Physiol Lung Cell Mol Physiol, June 1, 2005; 288(6): L1040 - L1048.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
H. Chen, O. Tliba, C. R. Van Besien, R. A. Panettieri Jr., and Y. Amrani
Selected Contribution: TNF-{alpha} modulates murine tracheal rings responsiveness to G-protein-coupled receptor agonists and KCl
J Appl Physiol, August 1, 2003; 95(2): 864 - 872.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2002 by the American Physiological Society.