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In cardiac myoblasts, cellular redox regulates FosB and Fra-1 through multiple cis-regulatory modules

Ekta Jindal1, Shyamal K Goswami

  • 1School of Life Sciences, Jawaharlal Nehru University, New Delhi 110067, India.

Free Radical Biology & Medicine
|August 9, 2011
PubMed

Insights

Norepinephrine (NE) triggers cardiac cell hypertrophy or apoptosis via reactive oxygen species (ROS), differentially regulating FosB and Fra-1 gene expression. ROS control of these genes is context-dependent, involving specific promoter elements like SP-1.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Cell Signaling

Background:

  • Norepinephrine (NE) induces cardiac myocyte hypertrophy or apoptosis.
  • Reactive oxygen species (ROS) mediate these NE-induced cellular responses.
  • FosB and Fra-1, AP-1 family transcription factors, are differentially regulated in these pathways.

Purpose of the Study:

  • To investigate the transcriptional regulation of fosB and fra-1 by NE and ROS.
  • To elucidate the mechanisms by which ROS control fosB and fra-1 expression.
  • To identify cis-elements and redox-sensitive transcription factors involved in gene regulation.

Main Methods:

  • Cloning of fosB and fra-1 upstream regions into luciferase vectors for transient expression assays.
  • Treatment with NE, catalase, and MnTMPyP to assess gene and promoter activity.
  • Deletion, mutation, ChIP, and gel mobility-shift assays to analyze cis-elements and protein-DNA interactions.

Main Results:

  • NE induced fosB and fra-1 transcription, which was suppressed by catalase and MnTMPyP.
  • ROS regulation of fosB and fra-1 was context-specific, differing between NE-treated and untreated cells.
  • SP-1, CEBP, and AP-1 cis-elements in the fosB promoter mediated redox responses, with SP-1 identified as a direct redox sensor.

Conclusions:

  • ROS-mediated regulation of fosB and fra-1 is context-dependent.
  • Multiple cis-elements and transcription factors contribute to redox-sensitive gene expression.
  • Gene-specific modules are generated by multiple redox signals, influencing gene expression in cardiac myocytes.

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