Advertisement
JBC

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Originally published In Press as doi:10.1074/jbc.M708025200 on November 9, 2007

J. Biol. Chem., Vol. 283, Issue 2, 1128-1136, January 11, 2008
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/2/1128    most recent
M708025200v1
Right arrow Submit a Letter to Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chen, Y.
Right arrow Articles by Xie, Z.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chen, Y.
Right arrow Articles by Xie, Z.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Regulation of Inositol 1,4,5-Trisphosphate Receptor-mediated Calcium Release by the Na/K-ATPase in Cultured Renal Epithelial Cells*

Ying Chen{ddagger}, Ting Cai{ddagger}, Changjun Yang{ddagger}, David A. Turner§, David R. Giovannucci§, and Zijian Xie{ddagger}1

From the {ddagger}Department of Physiology and Pharmacology and §Department of Neuroscience, University of Toledo, College of Medicine, Toledo, Ohio 43614

It is known that the Na/K-ATPase {alpha}1 subunit interacts directly with inositol 1,4,5-triphosphate (IP3) receptors. In this study we tested whether this interaction is required for extracellular stimuli to efficiently regulate endoplasmic reticulum (ER) Ca2+ release. Using cultured pig kidney LLC-PK1 cells as a model, we demonstrated that graded knockdown of the cellular Na/K-ATPase {alpha}1 subunit resulted in a parallel attenuation of ATP-induced ER Ca2+ release. When the knockdown cells were rescued by knocking in a rat {alpha}1, the expression of rat {alpha}1 restored not only the cellular Na/K-ATPase but also ATP-induced ER Ca2+ release. Mechanistically, this defect in ATP-induced ER Ca2+ release was neither due to the changes in the amount or the function of cellular IP3 and P2Y receptors nor the ER Ca2+ content. However, the {alpha}1 knockdown did redistribute cellular IP3 receptors. The pool of IP3 receptors that resided close to the plasma membrane was abolished. Because changes in the plasma membrane proximity could reduce the efficiency of signal transmission from P2Y receptors to the ER, we further determined the dose-dependent effects of ATP on protein kinase C{epsilon} activation and ER Ca2+ release. The data showed that the {alpha}1 knockdown de-sensitized the ATP-induced ER Ca2+ release but not PKC{epsilon} activation. Moreover, expression of the N terminus of Na/K-ATPase {alpha}1 subunit not only disrupted the formation of the Na/K-ATPase-IP3 receptor complex but also abolished the ATP-induced Ca2+ release. Finally, we observed that the {alpha}1 knockdown was also effective in attenuating ER Ca2+ release provoked by angiotensin II and epidermal growth factor.


Received for publication, September 25, 2007 , and in revised form, November 8, 2007.

* This work was supported by National Institutes of Health Grants HL-36573, HL-67963, and GM-78565 and by American Heart Association Grant 0130231N. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

1 To whom correspondence should be addressed: Dept. of Physiology and Pharmacology, the University of Toledo College of Medicine, 3035 Arlington Ave., Toledo, OH 43614-5804. Tel.: 419-383-4182; Fax: 419-383-2871; E-mail: Zi-Jian.Xie{at}utoledo.edu.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
Y. Chen, T. Cai, H. Wang, Z. Li, E. Loreaux, J. B. Lingrel, and Z. Xie
Regulation of Intracellular Cholesterol Distribution by Na/K-ATPase
J. Biol. Chem., May 29, 2009; 284(22): 14881 - 14890.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2008 by the American Society for Biochemistry and Molecular Biology.
Advertisement
spacer
Advertisement
Advertisement