Key result
Salusin-β silencing improved endothelium-dependent vasorelaxation, oxidative stress, and inflammatory response in diabetic aorta by restoring PPARγ expression.
Why the study?
Does salusin-β silencing improve endothelial dysfunction in models of diabetes mellitus?
Does salusin-β silencing improve endothelial dysfunction in models of diabetes mellitus?
Salusin-β silencing protects against diabetes-induced endothelial dysfunction by preventing the degradation of PPARγ, highlighting a potential therapeutic target for diabetic vascular complications.
Salusin-β inhibition improves endothelial function in diabetic mice; leaves open therapeutic relevance in patients.
The pathophysiological mechanisms for vascular lesions in diabetes mellitus (DM) are complex, among which endothelial dysfunction plays a vital role. Therapeutic target against endothelial injury may provide critical venues for treatment of diabetic vascular diseases. We recently identified that salusin‐β contributed to high glucose‐induced endothelial cell apoptosis. However, the roles of salusin‐β in DM‐induced endothelial dysfunction remain largely elusive. Male C57BL/6J mice were used to induce type 2 diabetes mellitus (T2DM) model. Human umbilical vein endothelial cells (HUVECs) were cultured in high glucose/high fat (HG/HF) medium. We demonstrated increased expression of salusin‐β in diabetic aortic tissues and high‐glucose/high‐fat‐ (HG/HF‐) incubated HUVECs. Disruption of salusin‐β by shRNA abrogated the reactive oxygen species (ROS) production, inflammation, and nitrotyrosine content of HUVECs cultured in HG/HF medium. The HG/HF‐mediated decrease in peroxisome proliferator‐activated receptor γ (PPARγ) expression was restored by salusin‐β shRNA, and PPARγ inhibitor T0070907 abolished the protective actions of salusin‐β shRNA on endothelial injury in HG/HF‐treated HUVECs. Salusin‐β silencing obviously improved endothelium‐dependent vasorelaxation, oxidative stress, inflammatory response, and nitrative stress in diabetic aorta. Taken together, our results highlighted the essential role of salusin‐β in pathological endothelial dysfunction, and salusin‐β may be a promising target in treatment of vascular complications of DM.
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Sun et al. (2017) studied Type 2 diabetes mellitus and endothelial dysfunction. Salusin-β silencing (shRNA) vs. Control (diabetic/HG-HF conditions without silencing) was evaluated on Endothelial dysfunction (ROS production, inflammation, nitrotyrosine content, vasorelaxation). Salusin-β silencing improved endothelium-dependent vasorelaxation, oxidative stress, and inflammatory response in diabetic aorta by restoring PPARγ expression.
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