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IGF\u2010IIR gene expression\/ suppression is able to prevent myocardial remodeling. However, the regulating mechanisms for the IGF\u2010IIR gene remain unclear. This study performed reverse transcriptase PCR (RT\u2010PCR) and methylation\u2010specific PCR (MS\u2010PCR) to detect expression and DNA methylation of CpG islands within the IGF\u2010IIR genomic DNA region. Our finding revealed that the IGF\u2010IIR gene was up\u2010regulated both in H9c2 cells treated with tumor necrosis factor\u2010alpha (TNF\u2010\u03b1), lipopolysaccharide (LPS), angiotensin II (ANGII) and inomycin, and age\u2010dependently in spontaneously hypertensive rat (SHR) heart. For the DNA methylation study, although there were four CpG islands within IGF\u2010IIR genomic regions, the DNA methylation distribution showed no change either in cells treated with ANGII or in the SHR heart. Using chemical inhibitors to individually block histone acetyltransferase (HAT) and histone deacetylase (HDAC) activity, we found that histone acetylation was essential for ANGII\u2010induced IGF\u2010IIR gene expression using RT\u2010PCR and luciferase assay. The Chromatin immuno\u2010precipitation assay indicated that acetyl\u2010Histone H3 and acetyl\u2010Histone H4 associated with the IGF\u2010IIR promoter increased in the presence of ANGII, otherwise methyl\u2010CpG binding domain protein 2 (MeCP2) is disassociated with this. Taken together, this study demonstrates that histone acetylation plays a critical role in IGF\u2010IIR up\u2010regulation during pathological cardiac diseases and might provide a targeting gene in transcriptional therapies for the failing heart. J. Cell. Physiol. 227: 259\u2013268, 2012. \u00a9 2011 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcp.22728","type":"journal-article","created":{"date-parts":[[2011,3,16]],"date-time":"2011-03-16T13:19:27Z","timestamp":1300281567000},"page":"259-268","source":"Crossref","is-referenced-by-count":40,"title":["Histone acetylation is essential for ANG\u2010II\u2010induced IGF\u2010IIR gene expression in H9c2 cardiomyoblast cells and pathologically hypertensive rat 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