Document Detail


Impaired cardiac contractility response to hemodynamic stress in S100A1-deficient mice.
MedLine Citation:
PMID:  11909974     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ca(2+) signaling plays a central role in cardiac contractility and adaptation to increased hemodynamic demand. We have generated mice with a targeted deletion of the S100A1 gene coding for the major cardiac isoform of the large multigenic S100 family of EF hand Ca(2+)-binding proteins. S100A1(-/-) mice have normal cardiac function under baseline conditions but have significantly reduced contraction rate and relaxation rate responses to beta-adrenergic stimulation that are associated with a reduced Ca(2+) sensitivity. In S100A1(-/-) mice, basal left-ventricular contractility deteriorated following 3-week pressure overload by thoracic aorta constriction despite a normal adaptive hypertrophy. Surprisingly, heterozygotes also had an impaired response to acute beta-adrenergic stimulation but maintained normal contractility in response to chronic pressure overload that coincided with S100A1 upregulation to wild-type levels. In contrast to other genetic models with impaired cardiac contractility, loss of S100A1 did not lead to cardiac hypertrophy or dilation in aged mice. The data demonstrate that high S100A1 protein levels are essential for the cardiac reserve and adaptation to acute and chronic hemodynamic stress in vivo.
Authors:
Xiao-Jun Du; Timothy J Cole; Nora Tenis; Xiao-Ming Gao; Frank Köntgen; Bruce E Kemp; Jörg Heierhorst
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Molecular and cellular biology     Volume:  22     ISSN:  0270-7306     ISO Abbreviation:  Mol. Cell. Biol.     Publication Date:  2002 Apr 
Date Detail:
Created Date:  2002-03-22     Completed Date:  2002-04-22     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  8109087     Medline TA:  Mol Cell Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2821-9     Citation Subset:  IM    
Affiliation:
Baker Medical Research Institute, Melbourne, Victoria 8008, Australia.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Agonists / pharmacology
Aging / physiology
Animals
Calcium Signaling / genetics,  physiology
Calcium-Binding Proteins / deficiency*,  genetics*,  physiology
Gene Targeting
Heart Ventricles / drug effects
Hemodynamics
Heterozygote
Isoproterenol / pharmacology
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Contraction / drug effects,  genetics,  physiology*
Receptors, Adrenergic, beta / physiology
S100 Proteins
Stress, Physiological / physiopathology
Ventricular Function
Chemical
Reg. No./Substance:
0/Adrenergic beta-Agonists; 0/Calcium-Binding Proteins; 0/Receptors, Adrenergic, beta; 0/S100 Proteins; 0/S100A1 protein; 7683-59-2/Isoproterenol
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