help button home button
AJRCMB
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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
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 Kinane, T. B.
Right arrow Articles by Ercolani, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kinane, T. B.
Right arrow Articles by Ercolani, L.

Am. J. Respir. Cell Mol. Biol., Volume 20, Number 1, January, 1999 35-42

Regulation of the G Protein Galpha i2 by Growth and Development in Fetal Airway Epithelium

T. Bernard Kinane, Katsumi Komatsuzaki, Maria D. Aleixo, Mary E. Sunday, and Louis Ercolani

Departments of Medicine and Pediatrics, Massachusetts General Hospital, and Harvard Medical School, Boston; and Departments of Pathology, Children's and Brigham & Women's Hospitals and Harvard Medical School, Boston, Massachusetts

Heterotrimeric guanine nucleotide-binding (G) proteins transduce a wide variety of receptor-mediated signals to effectors that are involved in numerous cellular functions, including cell proliferation and differentiation. Thrombin and bombesin/gastrin-releasing peptide mediate their effects via G protein-coupled receptors to regulate lung growth and development. The growth responses of these ligands are likely to be mediated via the Gi subfamily of G proteins, specifically via Galpha i2. We hypothesized that Galpha i2 is expressed in the lung during ontogeny in a growth-dependent manner, and that Galpha i2 regulates cell growth. We demonstrate that Galpha i2 is present in the developing lung of Sprague-Dawley rats, and that its expression is enhanced between embryonic Day 19 and postnatal Day 2. The strongest expression occurs in the fetal airway epithelium, and this expression in fetal airway cells is growth-dependent. Galpha i2 is localized to the plasma membrane, a location consistent with interaction with growth factor receptors. Inhibition of Gi-family signal transduction by pertussis toxin (10 ng/ml) inhibits DNA synthesis in embryonic Day 19 in fetal airway epithelium. Galpha i2 is likely to be a key mediator of growth signals in the developing lung.




This article has been cited by other articles:


Home page
 Am. J. Respir. Cell Mol. Bio.Home page
K. Mizuta, Y. Osawa, F. Mizuta, D. Xu, and C. W. Emala
Functional Expression of GABAB Receptors in Airway Epithelium
Am. J. Respir. Cell Mol. Biol., September 1, 2008; 39(3): 296 - 304.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
D. E. Kling, H. K. Lorenzo, A. M. Trbovich, T. B. Kinane, P. K. Donahoe, and J. J. Schnitzer
Pre- and Postnatal Lung Development, Maturation, and Plasticity: MEK-1/2 inhibition reduces branching morphogenesis and causes mesenchymal cell apoptosis in fetal rat lungs
Am J Physiol Lung Cell Mol Physiol, March 1, 2002; 282(3): L370 - L378.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 1999 American Thoracic Society. 		  2009/2010 ATS Fellows Career Development Awards