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Disturbance of cardiac gene expression and cardiomyocyte structure predisposes Mecp2-null mice to arrhythmias.
Hara, Munetsugu; Takahashi, Tomoyuki; Mitsumasu, Chiaki; Igata, Sachiyo; Takano, Makoto; Minami, Tomoko; Yasukawa, Hideo; Okayama, Satoko; Nakamura, Keiichiro; Okabe, Yasunori; Tanaka, Eiichiro; Takemura, Genzou; Kosai, Ken-ichiro; Yamashita, Yushiro; Matsuishi, Toyojiro.
Afiliación
  • Hara M; 1] Division of Gene Therapy and Regenerative Medicine, Cognitive and Molecular Research Institute of Brain Diseases [2] Department of Pediatrics, Kurume University School of Medicine, Kurume, Japan.
  • Takahashi T; 1] Division of Gene Therapy and Regenerative Medicine, Cognitive and Molecular Research Institute of Brain Diseases [2] Department of Pediatrics, Kurume University School of Medicine, Kurume, Japan.
  • Mitsumasu C; 1] Division of Gene Therapy and Regenerative Medicine, Cognitive and Molecular Research Institute of Brain Diseases [2] Department of Pediatrics, Kurume University School of Medicine, Kurume, Japan.
  • Igata S; Department of Physiology, Kurume University School of Medicine, Kurume, Japan.
  • Takano M; Department of Physiology, Kurume University School of Medicine, Kurume, Japan.
  • Minami T; Cardiovascular Research Institute, Kurume University, Kurume, Japan.
  • Yasukawa H; Cardiovascular Research Institute, Kurume University, Kurume, Japan.
  • Okayama S; Department of Anatomy, Kurume University School of Medicine, Kurume, Japan.
  • Nakamura K; Department of Anatomy, Kurume University School of Medicine, Kurume, Japan.
  • Okabe Y; 1] Division of Gene Therapy and Regenerative Medicine, Cognitive and Molecular Research Institute of Brain Diseases [2] Department of Physiology, Kurume University School of Medicine, Kurume, Japan.
  • Tanaka E; Department of Physiology, Kurume University School of Medicine, Kurume, Japan.
  • Takemura G; Department of Internal Medicine, Asahi University School of Dentistry, Gifu, Japan.
  • Kosai K; 1] Division of Gene Therapy and Regenerative Medicine, Cognitive and Molecular Research Institute of Brain Diseases [2] Department of Pediatrics, Kurume University School of Medicine, Kurume, Japan [3] Department of Gene Therapy and Regenerative Medicine, Advanced Therapeutics Course, Kagoshima Univ
  • Yamashita Y; Department of Pediatrics, Kurume University School of Medicine, Kurume, Japan.
  • Matsuishi T; 1] Division of Gene Therapy and Regenerative Medicine, Cognitive and Molecular Research Institute of Brain Diseases [2] Department of Pediatrics, Kurume University School of Medicine, Kurume, Japan.
Sci Rep ; 5: 11204, 2015 Jun 15.
Article en En | MEDLINE | ID: mdl-26073556
Methyl-CpG-binding protein 2 (MeCP2) is an epigenetic regulator of gene expression that is essential for normal brain development. Mutations in MeCP2 lead to disrupted neuronal function and can cause Rett syndrome (RTT), a neurodevelopmental disorder. Previous studies reported cardiac dysfunction, including arrhythmias in both RTT patients and animal models of RTT. In addition, recent studies indicate that MeCP2 may be involved in cardiac development and dysfunction, but its role in the developing and adult heart remains unknown. In this study, we found that Mecp2-null ESCs could differentiate into cardiomyocytes, but the development and further differentiation of cardiovascular progenitors were significantly affected in MeCP2 deficiency. In addition, we revealed that loss of MeCP2 led to dysregulation of endogenous cardiac genes and myocardial structural alterations, although Mecp2-null mice did not exhibit obvious cardiac functional abnormalities. Furthermore, we detected methylation of the CpG islands in the Tbx5 locus, and showed that MeCP2 could target these sequences. Taken together, these results suggest that MeCP2 is an important regulator of the gene-expression program responsible for maintaining normal cardiac development and cardiomyocyte structure.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Arritmias Cardíacas / Predisposición Genética a la Enfermedad / Miocitos Cardíacos / Epigénesis Genética / Proteína 2 de Unión a Metil-CpG / Miocardio Tipo de estudio: Prognostic_studies Límite: Animals / Female / Humans Idioma: En Revista: Sci Rep Año: 2015 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Arritmias Cardíacas / Predisposición Genética a la Enfermedad / Miocitos Cardíacos / Epigénesis Genética / Proteína 2 de Unión a Metil-CpG / Miocardio Tipo de estudio: Prognostic_studies Límite: Animals / Female / Humans Idioma: En Revista: Sci Rep Año: 2015 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Reino Unido