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Programmed Cell Death 5 Provides Negative Feedback on Cardiac Hypertrophy Through the Stabilization of

Jingjing Ye1, Qiaoxia Zheng2, Shi Jia1

  • 1From the Department of Physiology and Pathophysiology, School of Basic Medical Sciences (J.Y., S.J., X.Q., Y.C., C.X., L.W., L.Z., M.Z.), Peking University Health Science Center, Beijing, China.

Hypertension (Dallas, Tex. : 1979)
|October 26, 2018
PubMed

Insights

Programmed cell death 5 (PDCD5) protects the heart against hypertrophy by stabilizing SERCA2a protein. PDCD5 acts as a negative feedback mechanism, preventing excessive cardiac growth and dysfunction.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cellular Physiology

Background:

  • Programmed cell death 5 (PDCD5) is widely expressed, but its role in cardiac function remains unclear.
  • Cardiac hypertrophy is a significant risk factor for heart failure.

Purpose of the Study:

  • To elucidate the role of PDCD5 in the pathogenesis of cardiac hypertrophy.
  • To investigate the molecular mechanisms by which PDCD5 influences cardiac function.

Main Methods:

  • Utilized cardiac-specific PDCD5 knockout mice and cardiomyocyte models.
  • Analyzed protein expression, ubiquitination, and calcium handling.
  • Investigated the regulatory relationship between PDCD5, NFATc2, and SERCA2a.

Main Results:

  • PDCD5 deficiency led to severe cardiac hypertrophy, impaired function, and reduced SERCA2a levels.
  • PDCD5 protein levels increased in hypertrophic hearts and were regulated by NFATc2.
  • PDCD5 overexpression inhibited hypertrophy, while knockdown exacerbated it.
  • PDCD5 stabilized SERCA2a by preventing its ubiquitination, improving calcium handling and cardiac function.

Conclusions:

  • PDCD5 is a novel NFATc2 target in hypertrophic hearts.
  • PDCD5 acts as a protective factor against cardiac hypertrophy through SERCA2a stabilization.
  • PDCD5 represents a potential therapeutic target for treating cardiac hypertrophy.
Keywords:
calcium signalingendoplasmic reticulummice, knockoutmyocytes, cardiacphenylephrine

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