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Affixin (β-parvin) promotes cardioprotective signaling via STAT3 activation

Mark Luedde1, Saskia Spaich, Hans-Joerg Hippe

  • 1Department of Internal Medicine III, Cardiology and Angiology, University of Kiel, 24105 Kiel, Germany.

Journal of Molecular and Cellular Cardiology
|February 8, 2011
PubMed

Insights

The focal adhesion protein affixin activates signal transducer and activator of transcription 3 (STAT3) in heart cells. This promotes cardiomyocyte growth, survival, and blood vessel formation, suggesting new cardioprotective strategies.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cell Biology
  • Protein Interactions

Background:

  • Affixin (β-parvin), a focal adhesion protein, is abundant in cardiomyocytes.
  • Its precise function in heart cells, despite roles in adhesion and migration, is not fully understood.

Purpose of the Study:

  • To elucidate the functional role of affixin in cardiomyocytes.
  • To identify affixin's interaction partners and downstream signaling pathways.

Main Methods:

  • Yeast-two-hybrid screening to identify binding partners.
  • Overexpression of affixin in neonatal rat cardiomyocytes.
  • Assays for STAT3 DNA binding activity, gene expression, cell size, protein synthesis, apoptosis, and HUVEC tubuli formation.

Main Results:

  • Affixin was identified as a binding partner of signal transducer and activator of transcription 3 (STAT3).
  • Affixin overexpression enhanced STAT3 DNA binding activity and upregulated STAT3-dependent genes.
  • Increased affixin levels induced cardiomyocyte hypertrophy, enhanced protein synthesis, and protected against doxorubicin-induced apoptosis.
  • Conditioned media from affixin-overexpressing cardiomyocytes promoted HUVEC tubuli formation, indicating proangiogenic effects.

Conclusions:

  • Affixin activates STAT3 signaling in cardiomyocytes.
  • This activation mediates hypertrophy, anti-apoptosis, and proangiogenic effects.
  • The affixin-STAT3 pathway presents a potential target for cardioprotective therapies.

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