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Vascular endothelial growth factor ameliorated palmitate-induced cardiomyocyte injury via JNK pathway

Shi-Ya Wang1,2, Cao Zou1, Xiao-Feng Liu2

  • 1Department of Cardiology, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, , Jiangsu, China.

In Vitro Cellular & Developmental Biology. Animal
|November 18, 2021
PubMed

Insights

Vascular endothelial growth factor (VEGF) protects heart cells from saturated fatty acid damage. VEGF reduces programmed cell death in cardiomyocytes, offering a potential target for cardiovascular protection against fatty acid stress.

Area of Science:

  • Cardiovascular Biology
  • Cellular Stress Response
  • Molecular Cardiology

Background:

  • Saturated fatty acids (SFAs) induce cardiomyocyte apoptosis, contributing to myocardial infarction and cardiac dysfunction.
  • The protective role of vascular endothelial growth factor (VEGF) in mitigating SFA-induced cardiomyocyte injury remains unclear.

Purpose of the Study:

  • To investigate the protective effects of VEGF against ceramide-mediated programmed cell death in cardiomyocytes.
  • To establish an in vitro model of palmitate-induced cardiomyocyte injury using H9c2 cells.

Main Methods:

  • H9c2 cells were treated with palmitate (PAL) to induce injury.
  • VEGF overexpression was employed to assess its protective effects.
  • Apoptosis rates, cell viability, and the expression of key apoptotic factors (caspase 3, Bax, Bcl-2, NF-κB p65, JNK, ERK) were analyzed.

Main Results:

  • Palmitate treatment significantly reduced cell viability and increased apoptosis in a time-dependent manner.
  • VEGF overexpression restored cell viability and reduced apoptosis.
  • VEGF reduced the expression of caspase 3, Bax, and NF-κB p65, while increasing Bcl-2 and p-JNK/JNK levels.

Conclusions:

  • VEGF exhibits significant protective effects against ceramide-induced cardiomyocyte apoptosis caused by fatty acid stress.
  • VEGF may serve as a therapeutic target for cardiovascular protection in conditions involving fatty acid overload.

Keywords:
ApoptosisCardiomyocyteCaspase 3NF-κBPalmitateVEGF

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