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- Publisher
- The American Physiological Society
- Copyright
- Copyright © 2012 the American Physiological Society
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- DOI
- 10.1152/ajpheart.00457.2011
- pmid
- 22427521
- Publisher site
- See Article on Publisher Site
Abstract
Calsequestrin (CSQ) is a Ca 2+ storage protein that interacts with triadin (TRN), the ryanodine receptor (RyR), and junctin (JUN) to form a macromolecular tetrameric Ca 2+ signaling complex in the cardiac junctional sarcoplasmic reticulum (SR). Heart-specific overexpression of CSQ in transgenic mice (TG CSQ ) was associated with heart failure, attenuation of SR Ca 2+ release, and downregulation of associated junctional SR proteins, e.g., TRN. Hence, we tested whether co-overexpression of CSQ and TRN in mouse hearts (TG CxT ) could be beneficial for impaired intracellular Ca 2+ signaling and contractile function. Indeed, the depressed intracellular Ca 2+ concentration ((Ca) i ) peak amplitude in TG CSQ was normalized by co-overexpression in TG CxT myocytes. This effect was associated with changes in the expression of cardiac Ca 2+ regulatory proteins. For example, the protein level of the L-type Ca 2+ channel Ca v 1.2 was higher in TG CxT compared with TG CSQ . Sarco(endo)plasmic reticulum Ca 2+ -ATPase 2a (SERCA2a) expression was reduced in TG CxT compared with TG CSQ , whereas JUN expression and ( 3 H)ryanodine binding were lower in both TG CxT and TG CSQ compared with wild-type hearts. As a result of these expressional changes, the SR Ca 2+ load was higher in both TG CxT and TG CSQ myocytes. In contrast to the improved cellular Ca 2+ , transient co-overexpression of CSQ and TRN resulted in a reduced survival rate, an increased cardiac fibrosis, and a decreased basal contractility in catheterized mice, working heart preparations, and isolated myocytes. Echocardiographic and hemodynamic measurements revealed a depressed cardiac performance after isoproterenol application in TG CxT compared with TG CSQ . Our results suggest that co-overexpression of CSQ and TRN led to a normalization of the SR Ca 2+ release compared with TG CSQ mice but a depressed contractile function and survival rate probably due to cardiac fibrosis, a lower SERCA2a expression, and a blunted response to β-adrenergic stimulation. Thus the TRN-to-CSQ ratio is a critical modulator of the SR Ca 2+ signaling. contractility calcium signaling sarcoplasmic reticulum overexpression heart failure Copyright © 2012 the American Physiological Society « Previous | Next Article » Table of Contents This Article Published online before print March 16, 2012 , doi: 10.1152/ajpheart.00457.2011 AJP - Heart May 15, 2012 vol. 302 no. 10 H2008-H2017 » Abstract Free Full Text Free to you Full Text (PDF) Free to you All Versions of this Article: ajpheart.00457.2011v1 302/10/H2008 most recent Classifications Cardiac Excitation and Contraction Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Download to citation manager Citing Articles Load citing article information Citing articles via Web of Science Google Scholar Articles by Kučerová, D. Articles by Kirchhefer, U. PubMed PubMed citation Articles by Kučerová, D. Articles by Kirchhefer, U. Related Content Cardiac Excitation and Contraction Load related web page information Current Content Alert me to new issues of AJP - Heart About the Journal Information for Authors Submit a Manuscript Ethical Policies AuthorChoice PubMed Central Policy Reprints and Permissions Advertising Press Copyright © 2012 the American Physiological Society Print ISSN: 0363-6135 Online ISSN: 1522-1539 var gaJsHost = (("https:" == document.location.protocol) ? "https://ssl." : "http://www."); document.write(unescape("%3Cscript src='" + gaJsHost + "google-analytics.com/ga.js' type='text/javascript'%3E%3C/script%3E")); try { var pageTracker = _gat._getTracker("UA-2924550-1"); pageTracker._trackPageview(); } catch(err) {} var gaJsHost = (("https:" == document.location.protocol) ? "https://ssl." : "http://www."); document.write(unescape("%3Cscript src='" + gaJsHost + "google-analytics.com/ga.js' type='text/javascript'%3E%3C/script%3E")); try { var pageTracker = _gat._getTracker("UA-189672-30"); pageTracker._setDomainName(".physiology.org"); pageTracker._trackPageview(); } catch(err) {}
Journal
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: May 15, 2012