Document Detail


Constitutively active calcineurin induces cardiac endoplasmic reticulum stress and protects against apoptosis that is mediated by alpha-crystallin-B.
MedLine Citation:
PMID:  20937869     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cardiac-specific overexpression of a constitutively active form of calcineurin A (CNA) leads directly to cardiac hypertrophy in the CNA mouse model. Because cardiac hypertrophy is a prominent characteristic of many cardiomyopathies, we deduced that delineating the proteomic profile of ventricular tissue from this model might identify novel, widely applicable therapeutic targets. Proteomic analysis was carried out by subjecting fractionated cardiac samples from CNA mice and their WT littermates to gel-free liquid chromatography linked to shotgun tandem mass spectrometry. We identified 1,918 proteins with high confidence, of which 290 were differentially expressed. Microarray analysis of the same tissue provided us with alterations in the ventricular transcriptome. Because bioinformatic analyses of both the proteome and transcriptome demonstrated the up-regulation of endoplasmic reticulum stress, we validated its occurrence in adult CNA hearts through a series of immunoblots and RT-PCR analyses. Endoplasmic reticulum stress often leads to increased apoptosis, but apoptosis was minimal in CNA hearts, suggesting that activated calcineurin might protect against apoptosis. Indeed, the viability of cultured neonatal mouse cardiomyocytes (NCMs) from CNA mice was higher than WT after serum starvation, an apoptotic trigger. Proteomic data identified α-crystallin B (Cryab) as a potential mediator of this protective effect and we showed that silencing of Cryab via lentivector-mediated transduction of shRNAs in NCMs led to a significant reduction in NCM viability and loss of protection against apoptosis. The identification of Cryab as a downstream effector of calcineurin-induced protection against apoptosis will permit elucidation of its role in cardiac apoptosis and its potential as a therapeutic target.
Authors:
Nicolas Bousette; Shaan Chugh; Vincent Fong; Ruth Isserlin; Kyoung-Han Kim; Allen Volchuk; Peter H Backx; Peter Liu; Thomas Kislinger; David H MacLennan; Andrew Emili; Anthony O Gramolini
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-11
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  107     ISSN:  1091-6490     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-27     Completed Date:  2010-11-22     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  United States    
Other Details:
Languages:  eng     Pagination:  18481-6     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Toronto, Toronto, ON, Canada M5G 1A8.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology
Calcineurin / genetics,  metabolism*
Cardiomegaly / genetics,  metabolism,  pathology
Endoplasmic Reticulum / metabolism*
Gene Expression
Gene Expression Profiling
Gene Knockdown Techniques
Mice
Mice, Transgenic
Myocardium / cytology,  metabolism*
Protein Array Analysis
Proteomics
RNA, Small Interfering / genetics
Stress, Physiological
alpha-Crystallin B Chain / antagonists & inhibitors,  genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
MT 125450//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/RNA, Small Interfering; 0/alpha-Crystallin B Chain; EC 3.1.3.16/Calcineurin
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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