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Modulation of ventricular function through gene transfer in vivo

R J Hajjar1, U Schmidt, T Matsui

  • 1Cardiovascular Research Center and Heart Failure and Cardiac Transplantation Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA.

Proceedings of the National Academy of Sciences of the United States of America
|June 6, 1998
PubMed
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Cardiac gene transfer using adenoviral vectors successfully altered heart function in vivo. Overexpressing phospholamban (PL) in rat hearts reduced contractility and slowed relaxation, demonstrating potential for therapeutic applications.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Gene Therapy

Background:

  • Phospholamban (PL) is a key regulator of the sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), influencing cardiac contractility.
  • Altering PL expression offers a potential strategy to modulate cardiac function.

Purpose of the Study:

  • To investigate the feasibility and effects of in vivo cardiac gene transfer for altering cardiac function.
  • To examine the impact of phospholamban (PL) overexpression on rat heart function.

Main Methods:

  • Catheter-based delivery of recombinant adenoviral vectors carrying cDNA for PL, beta-galactosidase (beta-gal), or enhanced green fluorescent protein (EGFP) into rat hearts.
  • Assessment of PL protein levels via Western blot.
  • Evaluation of cardiac function, including peak left ventricular pressure, rate of pressure rise/fall, and relaxation time constant.

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Main Results:

  • Adenoviral vector-mediated PL overexpression increased PL levels by 2.8-fold in rat ventricles.
  • Overexpression of PL led to significantly reduced peak left ventricular pressure and impaired pressure development/relaxation.
  • The time constant of left ventricular relaxation was significantly increased in hearts overexpressing PL.

Conclusions:

  • Somatic gene transfer is a viable approach for generalized cardiac gene transfer in vivo.
  • Overexpression of phospholamban can effectively modulate cardiac function, reducing contractility and relaxation.
  • These findings support the potential of gene transfer strategies for experimental and therapeutic manipulation of cardiac function.