Document Detail


Reduced force production during low blood flow to the heart correlates with altered troponin I phosphorylation.
MedLine Citation:
PMID:  19507043     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A rat model of low myocardial blood flow was established to test the hypothesis that post-translational changes to proteins of the thin and thick muscle filaments correlate with decreased cardiac contractility. Following 3 days of low blood flow by constriction of the left anterior descending artery, rat hearts demonstrated a reduction in fractional shortening at rest and a relative decline in fractional shortening when challenged with high dose versus low dose dobutamine, reflecting reduced energy reserves. Permeabilized fibers from low blood flow hearts demonstrated a decline in maximum force per cross-section and Ca2+ sensitivity as compared to their sham operated counterparts. An examination of sarcomeric proteins by twodimensional gel electrophoresis, mass spectrometry, and phospho-specific antibodies provided evidence for Ser23/24 and Ser43/45 phosphorylation of troponin I (TnI). Total TnI phosphorylation was not different between the groups, but Ser23/24 phosphorylation declined with low blood flow, implying an accompanying increase in phosphorylation at other sites of TnI. Affinity chromatography demonstrated that TnI from low blood flow myocardium had reduced relative affinity to Ca2+ bound troponin C compared to TnI from sham operated hearts, providing a mechanism for reduced Ca2+ sensitivity of force production in low blood flow fibers. These findings suggest that altered TnI function, due to changes in the distribution of phosphorylated sites, is an early contributor to reduced contractility of the heart.
Authors:
Bridgette Christopher; Gresin O Pizarro; Bryson Nicholson; Samantha Yuen; Brian D Hoit; Ozgur Ogut
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-06-09
Journal Detail:
Title:  Journal of muscle research and cell motility     Volume:  30     ISSN:  1573-2657     ISO Abbreviation:  J. Muscle Res. Cell. Motil.     Publication Date:  2009  
Date Detail:
Created Date:  2009-08-28     Completed Date:  2009-11-02     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  8006298     Medline TA:  J Muscle Res Cell Motil     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  111-23     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, 44106, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Flow Velocity
Calcium / metabolism*
Cardiac Myosins / metabolism
Dobutamine / pharmacology
Heart / drug effects,  physiology*
Microfilaments / metabolism*
Myocardial Contraction / drug effects,  physiology*
Myosin Light Chains / metabolism
Phosphorylation
Rats
Troponin C / metabolism
Troponin I / metabolism*
Troponin T / metabolism
Grant Support
ID/Acronym/Agency:
R01 HL078845/HL/NHLBI NIH HHS; R01 HL078845-04/HL/NHLBI NIH HHS; T32 GM07250/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Myosin Light Chains; 0/Troponin C; 0/Troponin I; 0/Troponin T; 0/myosin light chain 2; 34368-04-2/Dobutamine; 7440-70-2/Calcium; EC 3.6.1.-/Cardiac Myosins
Comments/Corrections

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


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