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The Involvement of SWI/SNF chromatin remodeling enzymes in Transcriptional Regulation of Pathological Cardiac Hypertrophy
Author(s) -
Mehrotra Aanchal,
Serna Ivana L
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb93
Subject(s) - chromatin , chromatin remodeling , swi/snf , promoter , reprogramming , microbiology and biotechnology , biology , transcription factor , gene expression , epigenetics , regulation of gene expression , chromatin immunoprecipitation , nfat , muscle hypertrophy , transcription (linguistics) , gene , genetics , endocrinology , linguistics , philosophy
Pathological cardiac hypertrophy is characterized by transcriptional reprogramming of gene expression which involves certain chromatin modulators. Little is known about the chromatin modifications involved in hypertrophy. SWI/SNF chromatin remodeling enzymes are epigenetic modulators playing pertinent roles in gene regulation. To understand the involvement of various subunits in the SWI/SNF complex and to study the chromatin modifications occurring in hypertension induced cardiac hypertrophy, we performed expression analysis as well as chromatin immunoprecipitaions (CHIPs) on Dahl salt sensitive and resistant rat hearts. The relative protein expression revealed a significant increase of Brg1, Baf 60c and Baf 180 in sensitive rat hearts. Moreover CHIPs demonstrated an increased enrichment of these subunits on promoters of ANP and BNP (hypertrophic markers) in sensitive models. Also there was an increased relative enrichment of acetylated H4, H3K4 trimethylation (active transcription marks) and decreased enrichment of H3k9 trimethylation, H3k27 trimethylation (negative transcription marks) on ANP and BNP promoters in sensitive rats. Our studies for the first time revealed the importance of SWI/SNF complex in promoting cardiac hypertrophy in Dahl salt sensitive and resistant models and suggest what we believe to be a novel mechanism for reprogramming of gene expression involved in hypertrophy.