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  1. Home
  3. Research Domains
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  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Pim-1 Regulates Cardiomyocyte Survival Downstream Of Akt.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Pim-1 Regulates Cardiomyocyte Survival Downstream Of Akt.

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Pim-1 regulates cardiomyocyte survival downstream of Akt.

John A Muraski1, Marcello Rota, Yu Misao

  • 1San Diego State University Heart Institute, San Diego State University, 5500 Campanile Drive, San Diego, California 92182, USA.

Nature Medicine
|November 27, 2007

View abstract on PubMed

Summary
This summary is machine-generated.

Pim-1, a serine-threonine kinase, plays a vital role in heart protection. Its deficiency impairs cardiac function, while its overexpression enhances it, suggesting Pim-1 is crucial for cardioprotection downstream of Akt.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cellular Signaling

Background:

  • The serine-threonine kinases Pim-1 and Akt are key regulators of cell proliferation and survival.
  • While Akt's role in the myocardium is established, Pim-1's function in the heart remains largely unexplored.
  • Pim-1 expression declines during development but reappears after cardiac injury and is elevated in failing hearts.

Purpose of the Study:

  • To investigate the role of Pim-1 in cardiac protection and its relationship with Akt signaling.
  • To determine the impact of Pim-1 deficiency and overexpression on myocardial response to injury.

Main Methods:

  • Comparative analysis of Pim-1 expression in developing, injured, and failing hearts of mice and humans.
  • Assessment of cardiac function and survival in Pim-1-deficient and transgenic mice subjected to infarction or pressure overload.
  • Evaluation of cardiomyocyte apoptosis, protein levels (Bcl-2, Bcl-X(L), Bad), and calcium dynamics (SERCA2a) in different genetic backgrounds.

    • Main Results:

    • Pim-1-deficient mice showed impaired myocardial protection despite compensatory Akt activation after injury.
    • Transgenic overexpression of Pim-1 conferred protection against infarction injury.
    • Pim-1 inhibited cardiomyocyte apoptosis, increased anti-apoptotic proteins (Bcl-2, Bcl-X(L)), and enhanced Bad phosphorylation.
    • Pim-1 influenced calcium dynamics, increasing SERCA2a expression and enhancing calcium transients in overexpression models, while impairing them in deficient models.

    Conclusions:

    • Pim-1 is a critical mediator of cardioprotection, acting downstream of Akt signaling.
    • Pim-1 plays a significant role in regulating cardiomyocyte survival and cardiac function.
    • Modulation of Pim-1 expression represents a potential therapeutic strategy for heart disease.