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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
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.
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.
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