Abstract:
:Interleukin-18 (IL-18) elicited a robust hypertrophy response in H9c2 cardiomyocytes as judged by their accelerated rates of protein synthesis and increased cell size. Evidently, IL-18 treatment also induced a cardiac hypertrophy-specific program of gene expression in H9c2 cardiomyocytes since they elicited enhanced expression of atrial naturetic factor (ANF), desmin, and skeletal alpha-actin genes accompanied by a canonical switch in the transcription of alpha- and beta-myosin heavy chain (MyHC) genes. Co-treatment of H9c2 cells with m-carboxycinnamic acid bis-hydroxamide (CBHA), an inhibitor of histone deacetylases, significantly blocked both morphological and molecular manifestations of IL-18-induced cardiac hypertrophy in vitro. IL-18 treatment led to activation of phosphoinositide-3-kinase and phosphorylated Akt/protein kinase B, while CBHA blunted this pathway via inducing the expression of its upstream regulator, PTEN (phosphatase and tensin homolog). The architecture of bulk chromatin of H9c2 cells exposed to IL-18 and/or CBHA was significantly altered as judged by the extent of covalent modifications of its constituent histones. The chromatin immuno-precipitation (ChIP) assays revealed that IL-18-induced specific epigenetic changes in the chromatin of ANF, desmin, skeletal alpha-actin, and MyHC genes that were largely neutralized by CBHA. We demonstrate for the first time that 'histone code' of the entire approximately 50 kb genomic DNA encoding the alpha- and beta-MyHC genes and the intergenic DNA that generates anti-beta-MyHC RNA was uniquely modulated by pro- and anti-hypertrophy signals of IL-18 and CBHA, respectively.
journal_name
Mol Cell Biochemjournal_title
Molecular and cellular biochemistryauthors
Majumdar G,Johnson IM,Kale S,Raghow Rdoi
10.1007/s11010-008-9720-xsubject
Has Abstractpub_date
2008-05-01 00:00:00pages
47-60issue
1-2eissn
0300-8177issn
1573-4919journal_volume
312pub_type
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