Integration of microarray profiles associated with cardiomyopathy and the potential role of Ube3a in apoptosis

Mol Med Rep. 2014 Feb;9(2):621-5. doi: 10.3892/mmr.2013.1848. Epub 2013 Dec 9.

Abstract

Cardiomyopathy is the one of the primary causes of mortality. High‑throughput genome datasets provide novel information that aids the understanding of the complex mechanisms involved in cardiomyopathy. However, the causative mechanisms underlying cardiomyopathy are yet to be elucidated. In order to improve the use of the high‑throughput genome datasets, the present study employed 9 microarray datasets to mine for differentially expressed cardiomyopathy‑associated genes using bioinformatic methods. Following validation using quantitative polymerase chain reaction, ubiquitin‑protein ligase E3a (Ube3a) was selected as a candidate gene for the disease. Substantial evidence suggests that apoptosis may be involved in the pathophysiology of cardiomyopathies. Therefore, in the present study, H2O2 was utilized to induce apoptosis in H9C2 cells in order to understand the interrelation between Ube3a and the apoptosis-related protein p53. Ube3a and p53 were observed to be significantly increased at the transcriptional and translational levels in response to H2O2 treatment. The results of this study indicate the efficiency of the data integration and the significant interrelation between Ube3a and p53 in myocardial cells during apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / genetics*
  • Cardiomyopathies / genetics*
  • Cardiomyopathies / pathology
  • Computational Biology
  • Gene Expression Profiling*
  • Genome, Human
  • Humans
  • Hydrogen Peroxide / toxicity
  • Microarray Analysis
  • Oligonucleotide Array Sequence Analysis
  • Tumor Suppressor Protein p53
  • Ubiquitin-Protein Ligases / genetics*
  • Ubiquitin-Protein Ligases / metabolism

Substances

  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Hydrogen Peroxide
  • UBE3A protein, human
  • Ubiquitin-Protein Ligases