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Endoplasmic Reticulum Stress Drives VEGF Gene Expression in Monocytic Cells.

Fatemah Bahman1, Taha Nadeem2, Abdulrahman Alayyaf3

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Endoplasmic reticulum (ER) stress amplifies vascular endothelial growth factor (VEGF) in monocytic cells during metabolic stress. This occurs via reactive oxygen species (ROS), linking obesity, inflammation, and angiogenesis.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • Obesity is linked to chronic inflammation and oxidative stress, disrupting metabolic balance and increasing vascular endothelial growth factor (VEGF).
  • While hypoxia and fatty acids induce VEGF via oxidative stress, the role of endoplasmic reticulum (ER) stress in monocytic cells is not fully understood.

Purpose of the Study:

  • To investigate how ER stress interacts with metabolic stress to regulate VEGF expression in THP-1 monocytic cells.
  • To elucidate the mechanisms, including reactive oxygen species (ROS) production, involved in this interplay.

Main Methods:

  • THP-1 monocytic cells were subjected to metabolic stress using palmitic acid (PA) and ER stress using thapsigargin (TG).
  • VEGF mRNA and protein levels, ROS production, ER stress markers (CHOP, ATF6, IRE1), and antioxidant defense genes (SOD2, NRF2) were measured.
  • The effect of the antioxidant curcumin on VEGF expression and ROS was assessed.

Main Results:

  • Co-treatment with PA and TG significantly increased VEGF expression compared to PA alone.
  • This increase was associated with heightened ROS production and elevated ER stress markers.
  • Curcumin treatment reduced VEGF expression and ROS levels, confirming a ROS-dependent pathway.
  • Antioxidant defense gene expression (SOD2, NRF2) was upregulated, indicating a cellular response to oxidative stress.

Conclusions:

  • ER stress exacerbates VEGF induction in monocytic cells under lipotoxic conditions.
  • This amplification occurs through ROS-mediated pathways.
  • The findings suggest a mechanism connecting metabolic stress, inflammation, and angiogenesis in obesity-related disorders.