{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,3,9]],"date-time":"2024-03-09T05:26:59Z","timestamp":1709962019762},"reference-count":77,"publisher":"American Physiological Society","issue":"24","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiological Genomics"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:p> We investigated the genome-wide consequences of pan-histone deacetylase inhibitors (HDACIs) trichostatin A (TSA) and m-carboxycinnamic acid bis-hydroxamide (CBHA) in the hearts of BALB\/c mice eliciting hypertrophy in response to interleukin-18 (IL-18). Both TSA and CBHA profoundly altered cardiac chromatin structure that occurred concomitantly with normalization of IL-18-induced gene expression and amelioration of cardiac hypertrophy. The hearts of mice exposed to IL-18 +\/\u2212 TSA or CBHA elicited distinct gene expression profiles. Of 184 genes that were differentially regulated by IL-18 and TSA, 33 were regulated in an opposite manner. The hearts of mice treated with IL-18 and\/or CBHA elicited 147 differentially expressed genes (DEGs), a third of which were oppositely regulated by IL-18 and CBHA. Ingenuity Pathways and Kyoto Encyclopedia of Genes and Genomes analyses of DEGs showed that IL-18 impinged on TNF-\u03b1- and IFN\u03b3-specific gene networks relegated to controlling immunity and inflammation, cardiac metabolism and energetics, and cell proliferation and apoptosis. These TNF-\u03b1- and IFN\u03b3-specific gene networks, extensively connected with PI3K, MAPK, and NF-\u03baB signaling pathways, were oppositely regulated by IL-18 and pan-HDACIs. Evidently, both TSA and CBHA caused a two- to fourfold induction of phosphatase and tensin homolog expression to counteract IL-18-induced proinflammatory signaling and cardiac hypertrophy. <\/jats:p>","DOI":"10.1152\/physiolgenomics.00048.2011","type":"journal-article","created":{"date-parts":[[2011,9,28]],"date-time":"2011-09-28T01:20:31Z","timestamp":1317172831000},"page":"1319-1333","source":"Crossref","is-referenced-by-count":14,"title":["Panhistone deacetylase inhibitors inhibit proinflammatory signaling pathways to ameliorate interleukin-18-induced cardiac hypertrophy"],"prefix":"10.1152","volume":"43","author":[{"given":"Gipsy","family":"Majumdar","sequence":"first","affiliation":[{"name":"Department of Veterans Affairs Medical Center;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert J.","family":"Rooney","sequence":"additional","affiliation":[{"name":"Genome Explorations; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I. 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