Measuring adriamycin-induced cardiac hemodynamic dysfunction with a proteomics approach

Immunopharmacol Immunotoxicol. 2010 Sep;32(3):376-86. doi: 10.3109/08923970903440168.

Abstract

Adriamycin is a potent antitumor drug that causes severe cardiotoxicity. However, the toxic mechanisms are not clear. We used a proteomics approach to analyze changes in protein profiles after adriamycin-induced changes in hemodynamic factors. Although adriamycin itself did not affect left ventricular developed pressure (LVDP) or left ventricular end diastolic pressure (LVEDP), the drug did enhance susceptibility to ischemia-reperfusion-induced changes in LVDP, LVEDP and heart rate. Adriamycin altered the expression of 52 proteins, primarily energy metabolism and cytoskeleton proteins. Adriamycin decreased the expression of the metabolism-related proteins, ATP synthase, Sdha protein, Triose phosphate isomerase 1 (TPI-1), pyruvate dehydrogenase E1 alpha1, 6-phosphofructokinase, and fructose-1,6-bisphosphatase, as did cytoskeletal proteins, such as actin. Alterations in energy metabolism and subsequent free radical production may affect cytoskeletal protein expression, producing adriamycin-induced changes in cardiac hemodynamics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibiotics, Antineoplastic / adverse effects*
  • Antibiotics, Antineoplastic / pharmacology
  • Cytoskeleton / drug effects
  • Doxorubicin / adverse effects*
  • Doxorubicin / pharmacology
  • Energy Metabolism / drug effects
  • Heart / drug effects*
  • Heart / physiopathology
  • Hemodynamics / drug effects*
  • Male
  • Mice
  • Myocardial Reperfusion Injury / chemically induced*
  • Myocardial Reperfusion Injury / metabolism
  • Myocardial Reperfusion Injury / physiopathology
  • Proteins / analysis
  • Proteins / metabolism*
  • Proteomics
  • Ventricular Function, Left / drug effects

Substances

  • Antibiotics, Antineoplastic
  • Proteins
  • Doxorubicin