High glucose regulates LN expression in human liver sinusoidalendothelial cells through ROS/integrin v3 pathway
High glucose regulates LN expression in human liver sinusoidalendothelial cells through ROS/integrin v3 pathway
复制标题
高糖通过ROS/整合素v3途径调节人肝窦内皮细胞LN表达
DOI：
--
复制
发表时间：
2016
影响因子：
4.3
通讯作者：
Limin Tian
中科院分区：
文献类型：
--
作者：
Jing Liu;Jinxing Quan;Jing Feng;Qi Zhang;Yanjia Xu;Jia Liu;Wenhui Huang;Juxiang Liu;Limin Tian
糖尿病可引起多种血管并发症，是非酒精性脂肪性肝病（NAFLD）的主要危险因素之一。本研究旨在探讨高糖诱导人肝窦内皮细胞（HLSECs）内flaminin（LN）的表达及活性氧（ROS）和整合素v3在LN表达调控中的作用。在存在或不存在N-乙酰半胱氨酸（NAC）或克隆LM 609的情况下，用含有25 mM葡萄糖的培养基培养和处理HLSEC。用2，7-二氯荧光素二乙酸酯（DCFH-DA）探针检测HLSEC细胞内ROS水平。RT-PCR和Western blot检测整合素v3的表达，免疫荧光法检测LN的表达，与对照组相比，高糖组ROS水平升高，整合素v3和LN的表达增加。与高糖组相比，抗氧化剂NAC抑制了整合素v3的表达，NAC和整合素v3阻断抗体（克隆LM 609）下调了LN的表达。高糖通过ROS/integrin v3途径上调HLSEC中LN的表达。
tDiabetes mellitus can cause a wide variety of vascular complications and is one of the major risk factors forNon Alcoholic Fatty Liver Disease (NAFLD). The present study was designed investigate the expression oflaminin (LN) in human liver sinusoidal endothelial cells (HLSECs) induced by high glucose and the role ofreactive oxygen species (ROS) and integrin v3 in the regulation of LN expression. HLSECs were culturedand treated with media containing 25 mM glucose in the presence or absence of N-acetylcysteine (NAC)or clone LM609. The level of intracellular ROS of HLSECs was measured with 2,7dichloro-fluoresceindiacetate (DCFH-DA) probe. Expression of integrin v3 was measured using RT-PCR and Western blot.Expression of LN was testified by immunofluorescence assay.Compared with that in control group, ROS level and the expression of integrin v3 and LN increased inhigh glucose group. Compared with that in high glucose group, antioxidant NAC inhibited the expressionof integrin v3, NAC and the anti-body for blocking integrin v3 (clone LM609) down-regulated theexpression of LN. However, the above parameters did not differ between control and mannitol groups.High glucose up-regulates expression of LN in HLSECs through ROS/integrin v3 pathway.