Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.

Re-induction of fetal genes and/or re-expression of postnatal genes represent hallmarks of pathological cardiac remodeling, and are considered important in the progression of the normal heart towards heart failure (HF). Whether epigenetic modifications are involved in these processes is currently un...

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Autores principales:	Tiziana Angrisano, Gabriele Giacomo Schiattarella, Simona Keller, Gianluigi Pironti, Ermanno Florio, Fabio Magliulo, Roberta Bottino, Raffaela Pero, Francesca Lembo, Enrico Vittorio Avvedimento, Giovanni Esposito, Bruno Trimarco, Lorenzo Chiariotti, Cinzia Perrino
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e7d9e94f968949a0b3a3c17553245da1
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spelling	oai:doaj.org-article:e7d9e94f968949a0b3a3c17553245da12021-11-25T06:02:16ZEpigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.1932-620310.1371/journal.pone.0106024https://doaj.org/article/e7d9e94f968949a0b3a3c17553245da12014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25181347/?tool=EBIhttps://doaj.org/toc/1932-6203Re-induction of fetal genes and/or re-expression of postnatal genes represent hallmarks of pathological cardiac remodeling, and are considered important in the progression of the normal heart towards heart failure (HF). Whether epigenetic modifications are involved in these processes is currently under investigation. Here we hypothesized that histone chromatin modifications may underlie changes in the gene expression program during pressure overload-induced HF. We evaluated chromatin marks at the promoter regions of the sarcoplasmic reticulum Ca2+ATPase (SERCA-2A) and β-myosin-heavy chain (β-MHC) genes (Atp2a2 and Myh7, respectively) in murine hearts after one or eight weeks of pressure overload induced by transverse aortic constriction (TAC). As expected, all TAC hearts displayed a significant reduction in SERCA-2A and a significant induction of β-MHC mRNA levels. Interestingly, opposite histone H3 modifications were identified in the promoter regions of these genes after TAC, including H3 dimethylation (me2) at lysine (K) 4 (H3K4me2) and K9 (H3K9me2), H3 trimethylation (me3) at K27 (H3K27me3) and dimethylation (me2) at K36 (H3K36me2). Consistently, a significant reduction of lysine-specific demethylase KDM2A could be found after eight weeks of TAC at the Atp2a2 promoter. Moreover, opposite changes in the recruitment of DNA methylation machinery components (DNA methyltransferases DNMT1 and DNMT3b, and methyl CpG binding protein 2 MeCp2) were found at the Atp2a2 or Myh7 promoters after TAC. Taken together, these results suggest that epigenetic modifications may underlie gene expression reprogramming in the adult murine heart under conditions of pressure overload, and might be involved in the progression of the normal heart towards HF.Tiziana AngrisanoGabriele Giacomo SchiattarellaSimona KellerGianluigi PirontiErmanno FlorioFabio MagliuloRoberta BottinoRaffaela PeroFrancesca LemboEnrico Vittorio AvvedimentoGiovanni EspositoBruno TrimarcoLorenzo ChiariottiCinzia PerrinoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 9, p e106024 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Tiziana Angrisano Gabriele Giacomo Schiattarella Simona Keller Gianluigi Pironti Ermanno Florio Fabio Magliulo Roberta Bottino Raffaela Pero Francesca Lembo Enrico Vittorio Avvedimento Giovanni Esposito Bruno Trimarco Lorenzo Chiariotti Cinzia Perrino Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.
description	Re-induction of fetal genes and/or re-expression of postnatal genes represent hallmarks of pathological cardiac remodeling, and are considered important in the progression of the normal heart towards heart failure (HF). Whether epigenetic modifications are involved in these processes is currently under investigation. Here we hypothesized that histone chromatin modifications may underlie changes in the gene expression program during pressure overload-induced HF. We evaluated chromatin marks at the promoter regions of the sarcoplasmic reticulum Ca2+ATPase (SERCA-2A) and β-myosin-heavy chain (β-MHC) genes (Atp2a2 and Myh7, respectively) in murine hearts after one or eight weeks of pressure overload induced by transverse aortic constriction (TAC). As expected, all TAC hearts displayed a significant reduction in SERCA-2A and a significant induction of β-MHC mRNA levels. Interestingly, opposite histone H3 modifications were identified in the promoter regions of these genes after TAC, including H3 dimethylation (me2) at lysine (K) 4 (H3K4me2) and K9 (H3K9me2), H3 trimethylation (me3) at K27 (H3K27me3) and dimethylation (me2) at K36 (H3K36me2). Consistently, a significant reduction of lysine-specific demethylase KDM2A could be found after eight weeks of TAC at the Atp2a2 promoter. Moreover, opposite changes in the recruitment of DNA methylation machinery components (DNA methyltransferases DNMT1 and DNMT3b, and methyl CpG binding protein 2 MeCp2) were found at the Atp2a2 or Myh7 promoters after TAC. Taken together, these results suggest that epigenetic modifications may underlie gene expression reprogramming in the adult murine heart under conditions of pressure overload, and might be involved in the progression of the normal heart towards HF.
format	article
author	Tiziana Angrisano Gabriele Giacomo Schiattarella Simona Keller Gianluigi Pironti Ermanno Florio Fabio Magliulo Roberta Bottino Raffaela Pero Francesca Lembo Enrico Vittorio Avvedimento Giovanni Esposito Bruno Trimarco Lorenzo Chiariotti Cinzia Perrino
author_facet	Tiziana Angrisano Gabriele Giacomo Schiattarella Simona Keller Gianluigi Pironti Ermanno Florio Fabio Magliulo Roberta Bottino Raffaela Pero Francesca Lembo Enrico Vittorio Avvedimento Giovanni Esposito Bruno Trimarco Lorenzo Chiariotti Cinzia Perrino
author_sort	Tiziana Angrisano
title	Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.
title_short	Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.
title_full	Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.
title_fullStr	Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.
title_full_unstemmed	Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.
title_sort	epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/e7d9e94f968949a0b3a3c17553245da1
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Epigenetic switch at atp2a2 and myh7 gene promoters in pressure overload-induced heart failure.

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