Spatiotemporal expression of histone acetyltransferases p300 and CBP during mouse cardiogenesis

  • Jie Tian, Department of Cardiology, Children's Hospital of Chongqing Medical University, China
  • Guozhen Chen, Department of Cardiology, Children's Hospital of Chongqing Medical University, China
  • Jing Zhu, Department of Molecular Biology,Pediatric Institute of Chongqing Medical University, China
  • Gang Wu, Department of Cardiology, Children's Hospital of Chongqing Medical University, China
  • Huichao Sun, Department of Cardiology, Children's Hospital of Chongqing Medical University, China
  • Xupei Huang, Department of Biomedical Science, Charlie E. Schmidt College of Biomedical Science, Florida Atlantic University, United States
  • Objectives: The aim of this study was to analyze the protein distribution and mRNA expression levels of histone acetyltransferases p300 and CBP in mouse heart during embryonic development and in the adult heart.
    Methods: A total of 39 normal mouse embryonic hearts ranging in age from E7.5 to E18 as well as postnatal day 1 and adult hearts were used to analyze p300 and CBP protein distribution by immunohistochemistry. In addition, p300 and CBP mRNA levels were determined by RT–PCR using E10.5~E18 embryonic hearts as well as postnatal 1 day and adult hearts.
    Results: Immunohistochemical staining revealed that p300 was highly expressed in nearly every region of the hearts during different stages of embryonic development as well as in postnatal day 1 and adult hearts. No CBP expression was evident in E7.5 heart. However, CBP protein was detectable at the subseuqnt stages, but at a relatively low level. Examination of p300 and CBP mRNA levels showed a peak expression at stage E10.5 heart, which was gradually decreased during the subsequent embryonic development stages and throughout the postnatal to the adult stages.
    Conclusion: Our results demonstrate a dynamic expression pattern of p300 and CBP during mouse heart development, indicating that they may play an important role during cardiogenesis.