Differential expression of HDAC and HAT genes in atrophying skeletal muscle

ABSTRACT Introduction: Histone deacetylase (HDAC) proteins, which counter the activity of histone acetyltransferases (HATs), are necessary for normal muscle atrophy in response to several pathophysiological conditions. Despite this, it remains unknown whether a common or unique transcriptional profi...

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Bibliographic Details
Published inMuscle & nerve Vol. 52; no. 6; pp. 1098 - 1101
Main Authors Beharry, Adam W., Judge, Andrew R.
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.12.2015
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Summary:ABSTRACT Introduction: Histone deacetylase (HDAC) proteins, which counter the activity of histone acetyltransferases (HATs), are necessary for normal muscle atrophy in response to several pathophysiological conditions. Despite this, it remains unknown whether a common or unique transcriptional profile of HDAC and HAT genes exist during the progression of muscle atrophy. Methods: Muscles were harvested from cast immobilized, denervated, or nutrient deprived animals for quantitative reverse transcriptase‐polymerase chain reaction analysis of HDAC and HAT gene expression. Results: The mRNA levels of Hdac2, Hdac4, Hdac6, Sirt1, p300, Cbp, and Pcaf increased, and Hdac7 decreased in skeletal muscle in each experimental model of muscle atrophy. Hdac1 and Hdac3 were increased only in cast immobilized and denervated muscles. Conclusions: While specific HDACs and HATs are increased in multiple models of muscle atrophy, increased expression of class I HDACs was unique to muscle disuse, reinforcing that specific HDAC inhibitors may be more effective than pan‐HDAC inhibitors at countering muscle atrophy. Muscle Nerve 52: 1098–1101, 2015
Bibliography:ark:/67375/WNG-RB37HLZW-G
U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases - No. R01AR060209
istex:F0023B360FF971FECA8208BABCECCA97E85CA773
ArticleID:MUS24912
National Institute of Child Health and Human Development - No. Grant T32-HD-043730
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0148-639X
1097-4598
DOI:10.1002/mus.24912