High glucose and interleukin 1β-induced apoptosis in human umbilical vein endothelial cells involves in down-regulation of monocarboxylate transporter 4.
High glucose and interleukin 1β-induced apoptosis in human umbilical vein endothelial cells involves in down-regulation of monocarboxylate transporter 4.
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DOI：
10.1016/j.bbrc.2015.09.016
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发表时间：
2015-10
影响因子：
3.1
通讯作者：
Dong Wang;Qingjie Wang;G. Yan;Yong Qiao;Ling Sun;Boqian Zhu;Chengchun Tang;Yuchun Gu
中科院分区：
文献类型：
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作者：
Dong Wang;Qingjie Wang;G. Yan;Yong Qiao;Ling Sun;Boqian Zhu;Chengchun Tang;Yuchun Gu
高血糖和炎症可诱导血管内皮细胞凋亡，从而导致糖尿病血管并发症的发生。内皮细胞的能量代谢依赖于糖酵解，而单羧酸转运体(MCTs)通过调节乳酸的内流和外流来调节细胞内的pH。本研究旨在探讨MCT4在高糖(HG)和白介素1-β(IL-1β)诱导的人脐静脉内皮细胞(HUVECs)凋亡中的作用。我们用扫描离子电导显微镜(SICM)证实了大鼠主动脉内皮损伤严重。HG和IL-1β减少MCT4及其在质膜上的位置，增加乳酸蓄积和细胞凋亡。MCT4基因敲除可阻断乳酸外流，导致乳酸蓄积和pH下降，从而触发HUVECs的凋亡。
Hyperglycaemia and inflammatory can induce apoptosis in vascular endothelial cells, which contributes to the development of vascular complications in diabetes. Endothelial cells depend on glycolysis for their energy metabolism, and monocarboxylate transporters (MCTs) regulate intracellular pH by mediating the influx and efflux of lactate. Here, we evaluate the role of MCT4 in high glucose (HG) and interleukin 1β (IL-1β)-induced apoptosis in human umbilical vein endothelial cells (HUVECs). We demonstrate that aortic endothelium damage is severe indb/dbmice by using scanning ion conductance microscopy (SICM). HG and IL-1β decrease MCT4 and its location on plasma membrane, as well as increase lactic acid accumulation and apoptosis in HUVECs. Knockdown of MCT4 blocks lactate efflux to result in lactic acid accumulation and pH dropping, which is involved in triggering apoptosis in HUVECs.