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ERKs and JNKs mediate hydrogen peroxide-induced Egr-1 expression and nuclear accumulation in H9c2 cells

I K S Aggeli1, I Beis, C Gaitanaki

  • 1Department of Animal and Human Physiology, School of Biology, Faculty of Sciences, University of Athens, Athens, Greece.

Physiological Research
|August 18, 2009
PubMed

Insights

Hydrogen peroxide (H2O2) upregulates Early Growth Response factor-1 (Egr-1) in cardiac cells. This response is mediated by the ERK and JNK signaling pathways, affecting Egr-1 at mRNA, protein, and distribution levels.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cell Biology
  • Oxidative Stress Research

Background:

  • Cardiomyocyte homeostasis is threatened by reactive oxygen species (ROS) in heart failure.
  • Early Growth Response factor-1 (Egr-1) is a transcriptional regulator implicated in detrimental cardiomyocyte processes.
  • Understanding Egr-1 regulation by ROS is crucial for cardiac health.

Purpose of the Study:

  • To investigate the signaling pathways regulating Early Growth Response factor-1 (Egr-1) in response to hydrogen peroxide (H2O2).
  • To elucidate the role of Extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal kinases (JNKs) in H2O2-induced Egr-1 expression.

Main Methods:

  • H9c2 cardiac cells were treated with H2O2.
  • Egr-1 mRNA and protein levels were quantified over time.
  • Inhibitors of ERK (PD98059) and JNK (SP600125, AS601245) pathways were used.
  • Immunofluorescence microscopy assessed Egr-1 subcellular localization.

Main Results:

  • H2O2 treatment significantly induced Egr-1 mRNA and protein levels in H9c2 cells.
  • ERK and JNK pathway inhibition abolished H2O2-induced Egr-1 upregulation.
  • H2O2-induced nuclear translocation of Egr-1 was dependent on ERK and JNK signaling.

Conclusions:

  • ERK and JNK pathways are fundamental in regulating Egr-1 response to H2O2 in cardiac cells at multiple levels.
  • This study reveals a novel mechanism of Egr-1 regulation by oxidative stress in cardiomyocytes.
  • Further research is needed to determine Egr-1's precise physiological role in gene expression and cell fate.

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