|
|
|
|
A more recent version of this article appeared on September 1, 2003
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on December 2, 2002
Revised on May 1, 2003
Accepted on May 2, 2003
1 Division of Pulmonary and Critical Care Medicine
2 Division of Nephrology, Department of Medicine,
Northwestern University. Chicago, Illinois, 60611
* Corresponding author. E-mail address: e-lecuona{at}northwestern.edu.
The purpose of this study was to define the role of the Rho family
of small GTPases in the
-adrenergic regulation of the Na,K-ATPase in
alveolar epithelial cells (AEC). The
-adrenergic receptor agonist
isoproterenol (ISO) increased the Na,K-ATPase protein abundance at the
plasma membrane and activated RhoA in a time-dependent manner. AEC
pretreated with mevastatin, a specific inhibitor of prenylation, or
transfected with the dominant negative RhoAN19, prevented ISO-mediated
Na,K-ATPase exocytosis to the plasma membrane. The ISO-mediated
activation of RhoA in AEC occurred via
2-adrenergic
receptor activation of RhoA and involved Gs-PKA as
demonstrated by incubation with the PKA specific inhibitors H89 and PKI
(peptide specific inhibitor), and Gi, as incubation with
pertussis toxin or cells transfected with a minigene vector for
Gi inhibited the ISO-mediated RhoA activation. However,
cells transfected with minigene vectors for G12 and
G13 did not prevent RhoA activation by ISO. Finally, the
ISO-mediated Na,K-ATPase exocytosis was regulated by the Rho-associated
kinase (ROCK), as preincubation with the specific inhibitor Y-27632 or
transfection with dominant negative ROCK, prevented the increase in
Na,K-ATPase at the plasma membrane. Accordingly, ISO regulates
Na,K-ATPase exocytosis in alveolar epithelial cells via the activation
of
2-adrenergic receptor, Gs, PKA,
Gi, RhoA and ROCK.
This article has been cited by other articles:
![]() |
G. M. Mutlu and P. Factor Alveolar Epithelial 2-Adrenergic Receptors Am. J. Respir. Cell Mol. Biol., February 1, 2008; 38(2): 127 - 134. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. Schoner and G. Scheiner-Bobis Endogenous and exogenous cardiac glycosides: their roles in hypertension, salt metabolism, and cell growth Am J Physiol Cell Physiol, August 1, 2007; 293(2): C509 - C536. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Shen, M.-J. Lin, A. Yaradanakul, V. Lariccia, J. A. Hill, and D. W. Hilgemann Dual control of cardiac Na+ Ca2+ exchange by PIP2: analysis of the surface membrane fraction by extracellular cysteine PEGylation J. Physiol., August 1, 2007; 582(3): 1011 - 1026. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. A. Dada, E. Novoa, E. Lecuona, H. Sun, and J. I. Sznajder Role of the small GTPase RhoA in the hypoxia-induced decrease of plasma membrane Na,K-ATPase in A549 cells J. Cell Sci., July 1, 2007; 120(13): 2214 - 2222. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Lecuona, L. A. Dada, H. Sun, M. L. Butti, G. Zhou, T.-L. Chew, and J. I. Sznajder Na,K-ATPase {alpha}1-subunit dephosphorylation by protein phosphatase 2A is necessary for its recruitment to the plasma membrane FASEB J, December 1, 2006; 20(14): 2618 - 2620. [Abstract] [Full Text] [PDF] |
||||
![]() |
Z. S. Azzam, Y. Adir, L. Welch, J. Chen, J. Winaver, P. Factor, N. Krivoy, A. Hoffman, J. I. Sznajder, and Z. Abassi Alveolar fluid reabsorption is increased in rats with compensated heart failure Am J Physiol Lung Cell Mol Physiol, November 1, 2006; 291(5): L1094 - L1100. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Suzuki, Z.-G. Jin, D. F. Meoli, T. Matoba, and B. C. Berk Cyclophilin A Is Secreted by a Vesicular Pathway in Vascular Smooth Muscle Cells Circ. Res., March 31, 2006; 98(6): 811 - 817. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. M. Mutlu and J. I. Sznajder Mechanisms of pulmonary edema clearance Am J Physiol Lung Cell Mol Physiol, November 1, 2005; 289(5): L685 - L695. [Abstract] [Full Text] [PDF] |
||||