Document Detail


The δA isoform of calmodulin kinase II mediates pathological cardiac hypertrophy by interfering with the HDAC4-MEF2 signaling pathway.
MedLine Citation:
PMID:  21554860     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is a new promising target for prevention and treatment of cardiac hypertrophy and heart failure. There are three δ isoforms of CaMKII in the heart and previous studies focused primarily on δB and δC types. Here we report the δA isoform of CaMKII is also critically involved in cardiac hypertrophy. We found that δA was significantly upregulated in pathological cardiac hypertrophy in both neonatal and adult models. Upregulation of δA was accompanied by cell enlargement, sarcomere reorganization and reactivation of various hypertrophic cardiac genes including atrial natriuretic factor (ANF) and β-myocin heavy chain (β-MHC). Studies further indicated the pathological changes were largely blunted by silencing the δA gene and an underlying mechanism indicated selective interference with the HDAC4-MEF2 signaling pathway. These results provide new evidence for selective interfering cardiac hypertrophy and heart failure when CaMKII is considered as a therapeutic target.
Authors:
Changlin Li; Xiangyu Cai; Haili Sun; Ting Bai; Xilong Zheng; Xing Wang Zhou; Xiongwen Chen; Donald L Gill; Jing Li; Xiang D Tang
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-05-03
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  409     ISSN:  1090-2104     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-05-25     Completed Date:  2011-08-02     Revised Date:  2014-04-16    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  125-30     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium-Calmodulin-Dependent Protein Kinase Type 2 / biosynthesis*,  genetics
Cardiomegaly / genetics,  metabolism*,  pathology
Gene Silencing
Histone Deacetylases / genetics,  metabolism*
Isoenzymes / genetics,  metabolism
MADS Domain Proteins / metabolism*
MEF2 Transcription Factors
Myogenic Regulatory Factors / metabolism*
Rats
Rats, Sprague-Dawley
Signal Transduction
Up-Regulation
Grant Support
ID/Acronym/Agency:
AI058173/AI/NIAID NIH HHS; HL55426/HL/NHLBI NIH HHS; R01 AI058173/AI/NIAID NIH HHS; R01 AI058173-07/AI/NIAID NIH HHS; R01 HL055426/HL/NHLBI NIH HHS; R01 HL055426-09/HL/NHLBI NIH HHS; R01 HL088243/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Isoenzymes; 0/MADS Domain Proteins; 0/MEF2 Transcription Factors; 0/MEF2A protein, rat; 0/Myogenic Regulatory Factors; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 2.7.11.17/Camk2d protein, rat; EC 3.5.1.98/HDAC4 protein, rat; EC 3.5.1.98/Histone Deacetylases
Comments/Corrections

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