help button home button
AJRCMB
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Published ahead of print on March 30, 2006, doi:10.1165/rcmb.2006-0003OC
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2006-0003OCv1
35/2/243    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by White, T. A.
Right arrow Articles by Wylam, M. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by White, T. A.
Right arrow Articles by Wylam, M. E.
American Journal of Respiratory Cell and Molecular Biology. Vol. 35, pp. 243-251, 2006
© 2006 American Thoracic Society
DOI: 10.1165/rcmb.2006-0003OC

Role of Transient Receptor Potential C3 in TNF-{alpha}–Enhanced Calcium Influx in Human Airway Myocytes

Thomas A. White, Ailing Xue, Eduardo N. Chini, Michael Thompson, Gary C. Sieck and Mark E. Wylam

Departments of Allergy and Immunology, Medicine, Anesthesiology, and Physiology and Biomedical Engineering, College of Medicine, Mayo Clinic, Rochester, Minnesota

Correspondence and requests for reprints should be addressed to Mark E. Wylam, M.D., Division of Pulmonary and Critical Care, College of Medicine, Mayo Clinic and Foundation, Rochester, MN 55905. E-mail: wylam.mark{at}mayo.edu

Previous studies have suggested that the proinflammatory cytokine, TNF-{alpha}, contributes to airway hyperresponsivness by altering airway smooth muscle (ASM) Ca2+ responses to agonist stimulation. The present study examined the effects of TNF-{alpha} on Ca2+ influx pathways in cultured human ASM cells (HASMCs). Proteins encoded by the transient receptor potential (TRP) gene family function as channels through which receptor-operated and store-operated Ca2+ entry (SOCE) occur. In the present study, the presence of TRPC1, TRPC3, TRPC4, TRPC5, and TRPC6 mRNA and protein expression was confirmed in cultured HASMCs using RT-PCR and Western blot analysis. TNF-{alpha} treatment significantly increased TRPC3 mRNA and protein levels in HASMCs as well as SOCE. TNF-{alpha} treatment also increased both the peak and plateau intracellular Ca2+ concentration responses in HASMCs elicited by acetylcholine and bradykinin. The effects of TNF-{alpha} treatment on SOCE and agonist-induced intracellular Ca2+ concentration responses were attenuated using small interfering RNA transfection, which knocked down TRPC3 expression. Thus, in inflammatory airway diseases, TNF-{alpha} treatment may result in increased myocyte activation due to altered Ca2+ influx pathways. These results suggest that TRPC3 may be an important therapeutic target in inflammatory airway diseases such as asthma and chronic obstructive pulmonary disease.

Key Words: human airway smooth muscle • receptor-operated calcium entry • store-operated calcium entry • TNF-{alpha} • transient receptor potential channels




This article has been cited by other articles:


Home page
 Eur Respir JHome page
P. B. Helli and L. J. Janssen
Properties of a store-operated nonselective cation channel in airway smooth muscle
Eur. Respir. J., December 1, 2008; 32(6): 1529 - 1538.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
D. L. Clarke, A. Sutcliffe, K. Deacon, D. Bradbury, L. Corbett, and A. J. Knox
PKC{beta}II Augments NF-{kappa}B-Dependent Transcription at the CCL11 Promoter via p300/CBP-Associated Factor Recruitment and Histone H4 Acetylation
J. Immunol., September 1, 2008; 181(5): 3503 - 3514.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
D. Shan, R. B. Marchase, and J. C. Chatham
Overexpression of TRPC3 increases apoptosis but not necrosis in response to ischemia-reperfusion in adult mouse cardiomyocytes
Am J Physiol Cell Physiol, March 1, 2008; 294(3): C833 - C841.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
G. C. Sieck, T. A. White, M. A. Thompson, C. M. Pabelick, M. E. Wylam, and Y. S. Prakash
Regulation of store-operated Ca2+ entry by CD38 in human airway smooth muscle
Am J Physiol Lung Cell Mol Physiol, February 1, 2008; 294(2): L378 - L385.
[Abstract] [Full Text] [PDF]

Home page
 Proc Am Thorac SocHome page
J. A. Jude, M. E. Wylam, T. F. Walseth, and M. S. Kannan
Calcium Signaling in Airway Smooth Muscle
Proceedings of the ATS, January 1, 2008; 5(1): 15 - 22.
[Abstract] [Full Text] [PDF]

Home page
 Eur Respir JHome page
S. Hirota, P. Helli, and L. J. Janssen
Ionic mechanisms and Ca2+ handling in airway smooth muscle
Eur. Respir. J., July 1, 2007; 30(1): 114 - 133.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
J. M. Dai, K.-H. Kuo, J. M. Leo, P. D. Pare, C. van Breemen, and C.-H. Lee
Acetylcholine-Induced Asynchronous Calcium Waves in Intact Human Bronchial Muscle Bundle
Am. J. Respir. Cell Mol. Biol., May 1, 2007; 36(5): 600 - 608.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
Y. Amrani
TNF-{alpha} and Calcium Signaling in Airway Smooth Muscle Cells: A Never-Ending Story with Promising Therapeutic Relevance
Am. J. Respir. Cell Mol. Biol., March 1, 2007; 36(3): 387 - 388.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2006 American Thoracic Society. 		  2009/2010 ATS Fellows Career Development Awards