دورية أكاديمية
Epigenetic State Changes Underlie Metabolic Switch in Mouse Post-Infarction Border Zone Cardiomyocytes.
العنوان: | Epigenetic State Changes Underlie Metabolic Switch in Mouse Post-Infarction Border Zone Cardiomyocytes. |
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المؤلفون: | Günthel M; Department of Medical Biology, Amsterdam Cardiovascular Sciences, University of Amsterdam, Amsterdam University Medical Centers, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands., van Duijvenboden K; Department of Medical Biology, Amsterdam Cardiovascular Sciences, University of Amsterdam, Amsterdam University Medical Centers, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands., de Bakker DEM; Hubrecht Institute-KNAW, University Medical Center Utrecht, 3584 CT Utrecht, The Netherlands.; Leibniz Institute on Aging-Fritz Lipmann Institute, 07745 Jena, Germany., Hooijkaas IB; Department of Medical Biology, Amsterdam Cardiovascular Sciences, University of Amsterdam, Amsterdam University Medical Centers, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands., Bakkers J; Hubrecht Institute-KNAW, University Medical Center Utrecht, 3584 CT Utrecht, The Netherlands.; Department of Pediatric Cardiology, Division of Pediatrics, University Medical Center Utrecht, 3584 CX Utrecht, The Netherlands., Barnett P; Department of Medical Biology, Amsterdam Cardiovascular Sciences, University of Amsterdam, Amsterdam University Medical Centers, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands., Christoffels VM; Department of Medical Biology, Amsterdam Cardiovascular Sciences, University of Amsterdam, Amsterdam University Medical Centers, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands. |
المصدر: | Journal of cardiovascular development and disease [J Cardiovasc Dev Dis] 2021 Oct 22; Vol. 8 (11). Date of Electronic Publication: 2021 Oct 22. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: MDPI AG Country of Publication: Switzerland NLM ID: 101651414 Publication Model: Electronic Cited Medium: Internet ISSN: 2308-3425 (Electronic) Linking ISSN: 23083425 NLM ISO Abbreviation: J Cardiovasc Dev Dis Subsets: PubMed not MEDLINE |
أسماء مطبوعة: | Original Publication: Basel, Switzerland : MDPI AG |
مستخلص: | Myocardial infarction causes ventricular muscle loss and formation of scar tissue. The surviving myocardium in the border zone, located adjacent to the infarct, undergoes profound changes in function, structure and composition. How and to what extent these changes of border zone cardiomyocytes are regulated epigenetically is not fully understood. Here, we obtained transcriptomes of PCM-1-sorted mouse cardiomyocyte nuclei of healthy left ventricle and 7 days post myocardial infarction border zone tissue. We validated previously observed downregulation of genes involved in fatty acid metabolism, oxidative phosphorylation and mitochondrial function in border zone-derived cardiomyocytes, and observed a modest induction of genes involved in glycolysis, including Slc2a1 (Glut1) and Pfkp . To gain insight into the underlying epigenetic regulatory mechanisms, we performed H3K27ac profiling of healthy and border zone cardiomyocyte nuclei. We confirmed the switch from Mef2- to AP-1 chromatin association in border zone cardiomyocytes, and observed, in addition, an enrichment of PPAR/RXR binding motifs in the sites with reduced H3K27ac signal. We detected downregulation and accompanying epigenetic state changes at several key PPAR target genes including Ppargc1a (PGC-1α), Cpt2 , Ech1 , Fabpc3 and Vldrl in border zone cardiomyocytes. These data indicate that changes in epigenetic state and gene regulation underlie the maintained metabolic switch in border zone cardiomyocytes. |
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معلومات مُعتمدة: | COBRA3 Hartstichting; OUTREACH Hartstichting |
فهرسة مساهمة: | Keywords: H3K27ac; border zone; epigenetics; myocardial infarction; nuclear RNA-sequencing; transcriptome |
تواريخ الأحداث: | Date Created: 20211125 Latest Revision: 20240404 |
رمز التحديث: | 20240404 |
مُعرف محوري في PubMed: | PMC8620718 |
DOI: | 10.3390/jcdd8110134 |
PMID: | 34821687 |
قاعدة البيانات: | MEDLINE |
تدمد: | 2308-3425 |
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DOI: | 10.3390/jcdd8110134 |