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Notch1 signaling activation protected myocardium against hypoxia injury via reducing programmed cell death

Yongjun Hu1, Zhaofen Zheng1, Hongwei Pan1

  • 1Vasculocardiology Department of Hunan Provincial People's Hospital, Jiefang Road No.61, Changsha, China.

Pakistan Journal of Pharmaceutical Sciences
|December 1, 2017
PubMed

Insights

Notch1 activation protects heart cells from damage during oxygen deprivation. This study shows Notch1 reduces programmed cell death by altering key protein expressions, offering a potential therapeutic target for myocardial ischemia.

Area of Science:

  • Cardiovascular Biology
  • Cell Death Mechanisms
  • Molecular Cardiology

Background:

  • Programmed cell death is crucial for cardio protection.
  • Notch1 signaling is implicated in cell death pathways.
  • The specific role of Notch1 in myocardial ischemia is not fully understood.

Purpose of the Study:

  • To investigate the role of Notch1 in regulating programmed cell death in H9C2 myocardial cells under hypoxic conditions.
  • To determine if Notch1 activation can protect against hypoxia-induced apoptosis.

Main Methods:

  • H9C2 cells were transfected with Notch1 overexpression or siRNA plasmids.
  • Cells were subjected to hypoxia (1% oxygen for 12 hours).
  • Cell proliferation (MTS assay), apoptosis (flow cytometry), and gene/protein expression (RT-qPCR, Western Blot) of Caspase-3, Caspase-9, and Bcl-2 were analyzed.

Main Results:

  • Hypoxia decreased cell proliferation and Bcl-2 expression while increasing apoptosis, Caspase-3, and Caspase-9 expression.
  • Notch1 activation enhanced proliferation and Bcl-2 expression, concurrently reducing apoptosis, Caspase-3, and Caspase-9 expression.
  • Notch1 inhibition via siRNA produced opposite effects compared to Notch1 activation.

Conclusions:

  • Notch1 activation mitigates hypoxia-induced programmed cell death in myocardial cells.
  • Targeting Notch1 may offer a therapeutic strategy for myocardial ischemia by modulating apoptosis-related proteins (Caspase-3, Caspase-9, Bcl-2).

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