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Hypertrophic stimulation increases beta-actin dynamics in adult feline cardiomyocytes

Sundaravadivel Balasubramanian1, Santhosh K Mani, Harinath Kasiganesan

  • 1Cardiology Division, Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston, South Carolina, United States of America. balasubr@musc.edu

Plos One
|July 17, 2010
PubMed

Insights

Beta-actin plays a crucial role in cardiac cytoskeletal rearrangement and contractility during myocardial hypertrophy. This study reveals beta-actin

Area of Science:

  • Cardiovascular Biology
  • Cell Biology
  • Muscle Physiology

Background:

  • Myocardial hypertrophy is a response to hemodynamic stress, involving cellular growth.
  • The role of cytoskeletal elements, particularly beta-actin, in cardiomyocyte function during hypertrophy is not well understood.
  • Alpha-actin is known for its role in muscle contraction, but beta-actin's function in cardiomyocytes remains unclear.

Purpose of the Study:

  • To investigate the presence, distribution, and dynamics of beta-actin in adult cardiomyocytes under normal and hypertrophic conditions.
  • To determine the functional significance of beta-actin in cardiomyocyte contractility and cytoskeletal organization.
  • To explore beta-actin's role in cardiac cytoskeletal rearrangement during hypertrophic stimulation.

Main Methods:

  • Utilized a feline right ventricular pressure overload (RVPO) model.
  • Measured beta-actin levels and distribution using biochemical assays and microscopy.
  • Employed adenoviral expression of GFP-tagged beta-actin and fluorescence recovery after photobleaching (FRAP) to study dynamics.
  • Investigated the impact of beta-actin manipulation on cardiomyocyte contractility in vitro.

Main Results:

  • Beta-actin levels and its association with the Triton-insoluble fraction increased in pressure-overloaded myocardium.
  • Hypertrophic stimulation (in vivo RVPO, endothelin, or insulin) enhanced polymerized beta-actin (F-actin).
  • Exogenously expressed beta-actin localized to Z-discs, costameres, and cell termini, with dynamic exchange at Z-discs that accelerated upon stimulation.
  • Beta-actin overexpression improved, while its neutralization reduced, cardiomyocyte contractility.

Conclusions:

  • Beta-actin is present and dynamically active in adult cardiomyocytes, localizing to key cytoskeletal structures.
  • Beta-actin dynamics are altered during hypertrophic stimulation, suggesting its involvement in cardiac remodeling.
  • Beta-actin contributes to cardiomyocyte contractility and is a potential marker for cardiac cytoskeletal changes during hypertrophy.

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