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SENP3 regulates high glucose-induced endothelial dysfunction via ROS dependent signaling.

Fuheng Chen1, Dongdong Ma1, Aizhong Li1

  • 1Department of Cardiology, Shanxi Provincial People's Hospital, Taiyuan, Shanxi, China.

Diabetes & Vascular Disease Research
|November 24, 2020
PubMed
Summary

SENP3 plays a key role in high glucose-induced endothelial dysfunction. Its involvement is linked to reactive oxygen species (ROS) signaling pathways, impacting cell viability and adhesion.

Keywords:
ROSSENP3diabetes mellitusendothelial dysfunctionhigh glucose

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Endothelial cell dysfunction is a critical factor in diabetic complications.
  • High glucose levels are known to induce oxidative stress and impair endothelial function.

Purpose of the Study:

  • To investigate the role of SUMO-sentisase 3 (SENP3) in high glucose-induced endothelial cell dysfunction.
  • To elucidate the underlying mechanisms, particularly the involvement of reactive oxygen species (ROS) signaling.

Main Methods:

  • Quantitative PCR and western blotting to assess SENP3 expression in high glucose-cultured human aortic endothelial cells (HAECs).
  • In vitro knockdown of SENP3 to evaluate its effects on HAEC viability, apoptosis, migration, and endothelial-monocyte adhesion.
  • Establishment of a mouse model of type I diabetes to assess SENP3 expression in vivo.
  • Investigation of SENP3's effects on ROS-related signaling pathways in HAECs.

Main Results:

  • SENP3 mRNA and protein levels were significantly increased in high glucose-cultured HAECs in a time-dependent manner.
  • SENP3 knockdown reversed high glucose-induced reductions in HAEC viability, apoptosis, and migration.
  • SENP3 knockdown attenuated high glucose-induced endothelial-monocyte adhesion by downregulating ICAM-1 and VCAM-1 expression.
  • Increased SENP3, ICAM-1, and VCAM-1 expression was observed in the aorta of diabetic mice.
  • SENP3 expression was downregulated in HAECs treated with ROS scavengers or NOX4 siRNA.

Conclusions:

  • SENP3 is implicated in high glucose-induced endothelial dysfunction.
  • Reactive oxygen species (ROS)-dependent signaling pathways mediate the role of SENP3 in this process.