The expression of overexpressed PTEN enhanced IR-induced apoptosis of myocardial cells

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Y-B Zhu1, N Ding, H-L Yi

  • 1Department of Cardiovascular Surgery II, Beijing Children's ospital, Capital Medical University, National Center for Children's Health, Beijing, China. chongdejia8865na@126.com.

European Review for Medical and Pharmacological Sciences
|June 8, 2019
PubMed
Abstract

Insights

PTEN overexpression worsens heart cell apoptosis after ischemia-reperfusion injury. Blocking PTEN activates the PI3K/Akt pathway, reducing this cell death and protecting the heart.

Area of Science:

  • Cardiovascular Biology
  • Cellular Signaling
  • Molecular Medicine

Background:

  • Myocardial ischemia-reperfusion (I/R) injury is a significant cause of heart damage.
  • Myocardial cell apoptosis plays a crucial role in the pathology of I/R injury.
  • The PI3K/Akt signaling pathway is vital for cell survival and apoptosis regulation, offering potential therapeutic targets.

Purpose of the Study:

  • To investigate the role of PTEN in regulating the PI3K/Akt signaling pathway in myocardial I/R injury.
  • To explore the therapeutic potential of targeting PTEN in mitigating I/R-induced cardiac damage.

Main Methods:

  • Established rat myocardial I/R injury and H9C2 cell I/R models.
  • Assessed PTEN, p-Akt, Bcl-2, and Bax protein expression levels.
  • Quantified apoptosis using flow cytometry.
  • Utilized PTEN overexpression and inhibition strategies.

Main Results:

  • I/R injury led to increased PTEN and Bax, decreased p-Akt and Bcl-2, and enhanced apoptosis.
  • PTEN overexpression exacerbated apoptosis and suppressed the PI3K/Akt pathway.
  • PTEN inhibition activated PI3K/Akt signaling, reducing apoptosis and Bax, while increasing Bcl-2.

Conclusions:

  • PTEN acts as a negative regulator of the PI3K/Akt pathway in myocardial I/R injury.
  • Overexpression of PTEN aggravates myocardial cell apoptosis.
  • Inhibiting PTEN protects against I/R injury by activating the PI3K/Akt pathway and reducing apoptosis.

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