Neuronal p60TRP expression modulates cardiac capacity

J Proteomics. 2012 Feb 16;75(5):1600-17. doi: 10.1016/j.jprot.2011.11.034. Epub 2011 Dec 6.


Heart failure, including myocardial infarction, is the leading cause for death and the incidence of cardiovascular diseases is predicted to continue to rise worldwide. In the present study we investigated the whole heart proteome profile of transgenic p60-Transcription Regulator Protein (p60TRP) mice to gain an insight into the molecular events caused by the long-term effect of neural p60TRP over-expression on cardiac proteome changes and its potential implication for cardiovascular functions. Using an iTRAQ (isobaric tags for relative and absolute quantitation)-based proteomics research approach, we identified 1148 proteins, out of which 116 were found to be significantly altered in the heart of neural transgenic p60TRP mice. Based on the observed data, we conclude that in vivo neural over-expression of transgenic p60TRP with its neuroprotective therapeutic potential significantly affects cardiovascular capacities.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Basic Helix-Loop-Helix Transcription Factors / biosynthesis*
  • Basic Helix-Loop-Helix Transcription Factors / genetics
  • Gene Expression Regulation / genetics
  • Heart Failure / genetics
  • Heart Failure / metabolism*
  • Heart Failure / therapy
  • Humans
  • Mice
  • Mice, Transgenic
  • Muscle Proteins / genetics
  • Muscle Proteins / metabolism*
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Nerve Tissue Proteins / biosynthesis*
  • Nerve Tissue Proteins / genetics
  • Proteome / genetics
  • Proteome / metabolism*


  • Basic Helix-Loop-Helix Transcription Factors
  • Muscle Proteins
  • Nerve Tissue Proteins
  • Proteome