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TRAIL protects against endothelium injury in diabetes via Akt-eNOS signaling
Min Liu1, Guangda Xiang1, Junyan Lu1
1Department of Endocrinology, Wuhan General Hospital of Guangzhou Command, Wuluo Road 627, Wuhan 430070, Hubei Province, China.
Objective:
Although some studies have suggested that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) might be involved in atherosclerosis, its potential role in endothelial dysfunction and apoptosis has not been investigated. The aim of this study was to evaluate the impact of TRAIL on endothelium injury in diabetes and the underlying mechanism involved.
Methods:
Experimental diabetes was induced using streptozotocin in rats. Cohorts of diabetic rats received an intraperitoneal injection of recombinant TRAIL (rTRAIL) 20 μg per rat weekly for 6 weeks. Endothelial function was assessed by acetylcholine (Ach)-induced endothelium-dependent vasorelaxation using aortic rings. The antiapoptotic effects of TRAIL and its possible mechanisms were investigated in cultured human umbilical vein endothelial cells (HUVECs).
Results:
Experimental diabetes attenuated endothelial function, which was significantly improved by rTRAIL treatment (63.5 ± 4.62% vs. 78.4 ± 2.79%, P < 0.01). In cultured HUVECs, TRAIL suppressed high glucose-induced reactive oxygen species (ROS) production and cellular apoptosis, as well as the production of NADPH oxidase. Furthermore, the antiapoptotic actions of TRAIL were accompanied by Akt and endothelial nitric oxide synthase (eNOS) phosphorylation, as well as increased NO production.
Conclusions:
These findings indicate a novel role of TRAIL in the protection against vascular injury in diabetes. The protective effects of TRAIL are dependent on the activation of Akt-dependent eNOS signaling.
Insights
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) protects against vascular injury in diabetes by improving endothelial function. TRAIL reduces oxidative stress and apoptosis via Akt-dependent endothelial nitric oxide synthase signaling.
Area of Science:
- Vascular Biology
- Endocrinology
- Molecular Medicine
Background:
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been implicated in atherosclerosis.
- The role of TRAIL in diabetes-associated endothelial dysfunction and apoptosis remains unclear.
Purpose of the Study:
- To investigate the impact of TRAIL on endothelial injury in a diabetic model.
- To elucidate the underlying mechanisms of TRAIL's effects on endothelium.
Main Methods:
- Experimental diabetes induced in rats using streptozotocin.
- Diabetic rats treated with recombinant TRAIL (rTRAIL) to assess endothelial function via vasorelaxation.
- Human umbilical vein endothelial cells (HUVECs) used to study TRAIL's antiapoptotic effects and molecular pathways.
Main Results:
- Diabetes impaired endothelial function, which rTRAIL treatment significantly improved.
- TRAIL suppressed high glucose-induced reactive oxygen species (ROS) and apoptosis in HUVECs.
- TRAIL promoted Akt and eNOS phosphorylation, increasing nitric oxide (NO) production.
Conclusions:
- TRAIL plays a protective role against vascular injury in diabetes.
- TRAIL's protective effects are mediated by the activation of Akt-dependent eNOS signaling pathway.
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