SET8 is involved in the regulation of hyperglycemic memory in human umbilical endothelial cells

Acta Biochimica Et Biophysica Sinica
Xiangyuan ChenMinmin Zhu

Abstract

Hyperglycemic memory occurs in diabetic cardiovascular complications, but the underlying mechanism remains to be elucidated. Although the depletion of SET8 leads to increased mitochondrial oxidative stress via increasing cellular reactive oxygen species (ROS) production, the role of SET8 in hyperglycemic memory-induced mitochondrial dysfunction is not well understood. Here, we investigated the role of SET8 in this setting. Our results showed that high glucose-induced vascular inflammation, ROS production and apoptosis remained at high levels even when glucose returned to normal level. Elevated glucose reduced SET8 expression, which also remained at low level after returning to normoglycemia. SET8 overexpression protected cells from elevated glucose and hyperglycemic memory-induced endothelial injury by blocking ROS accumulation, attenuating vascular inflammation, and restoring nitric oxide production. Thus, our results suggest that SET8 may be a key mediator in hyperglycemic memory.

Citations

May 23, 2020·Cell Death & Disease·Jing WangChanghong Miao
Apr 11, 2020·Oxidative Medicine and Cellular Longevity·Jie QiChanghong Miao
May 16, 2021·Journal of Gastroenterology and Hepatology·Ping ChenMei Ye
Dec 19, 2021·Frontiers of Medicine·Jiabing ZhanHuaping Li

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