Salusin-β mediates high glucose-induced endothelial injury via disruption of AMPK signaling pathway.

The dysregulated proliferation, migration, apoptosis and angiogenesis of endothelial cells are involved in diabetic endothelial dysfunction. The circulating salusin-β levels were increased in diabetic patients, and salusin-β contributes to diabetic cardiomyopathy in rats. However, the roles of salusin-β in diabetes mellitus-induced endothelial dysfunction are not fully understood. Herein, we demonstrated the increased expressions of salusin-β in human umbilical vein endothelial cells (HUVECs) cultured in HG medium. Exposure of HUVECs to HG inhibited the proliferation, migration, and angiogenesis, retarded cell cycle progression of endothelial cells, which were rescued by knockdown of salusin-β. We also established that silencing of salusin-β with adenoviruse-mediated shRNA reduced high glucose-induced apoptosis by up-regulating Bcl-2 expression and down-regulating Bax and caspase-3 expressions. Blockade of salusin-β ameliorated HG-induced suppression of adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. Of note, pretreatment with AMPK inhibitor Compound C abolished salusin-β silencing-mediated endothelial protective effects. In summary, our results highlighted the involvement of salusin-β in HG-related endothelial dysfunction, and salusin-β contributed high glucose-induced endothelial injury via inactivation of AMPK signaling pathway.