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Aberrant expression profiles of isoproterenol-induced endoplasmic reticulum stress response genes in mouse myocardium

Lin Chen1, Weiguang Zhang, Juan He

  • 1Department of Biochemistry and Molecular Biology, Basic Medical Science College, Harbin Medical University, Harbin 150081, People's Republic of China.

Journal of Biochemical and Molecular Toxicology
|August 9, 2011
PubMed

Insights

This study reveals how endoplasmic reticulum (ER) stress genes respond to isoproterenol (ISO) in mouse hearts. While some ER stress responses protect cardiac cells, others lead to early apoptosis during ISO-induced cardiotoxicity.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Cellular Stress Response

Background:

  • Isoproterenol (ISO) induces acute cardiotoxicity, involving complex cellular stress pathways.
  • Endoplasmic reticulum (ER) stress is implicated in various cardiac pathologies.
  • Understanding ER stress gene regulation is crucial for managing cardiotoxicity.

Purpose of the Study:

  • To identify and characterize the expression profiles of ER stress response genes in ISO-induced cardiotoxicity.
  • To elucidate the functional roles of these genes in myocardial response to acute stress.
  • To investigate the mechanisms of cell survival and apoptosis under ISO-induced ER stress.

Main Methods:

  • Whole genome oligo microarrays were employed to analyze gene expression in damaged mouse cardiac tissues.
  • Mouse models were subjected to ISO administration for 6, 12, and 24 hours.
  • Functional analysis was performed on significantly altered ER stress-related genes.

Main Results:

  • Aberrant expression profiles of 26 ER stress-related genes were identified in ISO-treated mouse myocardium.
  • Functional analysis indicated cellular protective mechanisms including enhanced protein folding and inhibited translation.
  • Early-stage ER stress following ISO induction resulted in apoptosis in some myocardial cells.

Conclusions:

  • ISO-induced cardiotoxicity involves significant alterations in ER stress gene expression.
  • Myocardial cells activate protective pathways to cope with ER stress, but apoptosis can occur.
  • These findings provide insights into the molecular mechanisms of catecholamine-induced cardiac damage.

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