Hyperglycemia initiates N-cadherin rearrangement and diabetic monocytes promote inflammatory responses in human microvascular endothelial cells

Chi-Lun Feng, Hsiu-Chuan Chou
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引用次数: 2

Abstract

The prevalence of diabetes around the world is increasing, and the complications of diabetes are becoming worse so that the global burden of diabetes-related complications is rising. The purpose of this study was to simulate the physiological condition of diabetes in the human body by culturing human microvascular endothelial cell 1 (HMEC-1) cells in Dulbecco’s modified Eagle’s medium (DMEM) containing 5.5mM glucose, 25mM glucose, and 50mM glucose. The cell viability of HMEC-1 cells at the indicated glucose concentrations was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The specific epithelial cell junction N-cadherin was measured by immunofluorescence. Furthermore, monocytic initiation of inflammatory reactions was studied by using Western blotting and enzyme-linked immunosorbent assay. Based on our results, hyperglycemia treatment influenced the distribution of N-cadherin-containing structures in HMEC-1 cells, whereas the change of the inflammatory profiles in HMEC-1 cells was affected after their coculture with the supernatant of diabetic THP-1 monocytes. In this study, we conclude that the removal of endothelial N-cadherin caused by hyperglycemia (at the 25mM glucose and 50mM glucose concentrations) may lead to endothelial dysfunction and subsequently endothelial cell death in the late stage of diabetes. Furthermore, the loss of intercellular adhesion molecule 1 and the upregulation of interleukin (IL)-1, IL-6, and tumor necrosis factor alpha mediated by diabetic monocytes showed altered interaction between the vascular endothelium and blood cells in the diabetic microenvironment.

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高血糖引发n -钙粘蛋白重排,糖尿病单核细胞促进人微血管内皮细胞的炎症反应
世界各地的糖尿病患病率正在上升,糖尿病并发症正在恶化,因此全球糖尿病相关并发症的负担正在上升。本研究的目的是通过在含有5.5mM葡萄糖、25mM葡萄糖和50mM葡萄糖的Dulbecco 's modified Eagle 's medium (DMEM)中培养人微血管内皮细胞1 (HMEC-1)细胞,模拟人糖尿病的生理状态。采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑(MTT)法检测葡萄糖浓度下HMEC-1细胞的细胞活力。免疫荧光法检测特异性上皮细胞连接处n -钙粘蛋白。此外,用Western blotting和酶联免疫吸附法研究单核细胞引发炎症反应。根据我们的研究结果,高血糖治疗影响了HMEC-1细胞中含n-钙粘蛋白结构的分布,而HMEC-1细胞与糖尿病THP-1单核细胞的上清共培养后,炎症谱的变化受到影响。在本研究中,我们得出结论,在糖尿病晚期,由高血糖引起的内皮n -钙粘蛋白的去除(在25mM葡萄糖和50mM葡萄糖浓度下)可能导致内皮功能障碍并随后导致内皮细胞死亡。此外,糖尿病单核细胞介导的细胞间粘附分子1的缺失和白细胞介素(IL)-1、IL-6和肿瘤坏死因子α的上调表明,糖尿病微环境中血管内皮和血细胞之间的相互作用发生了改变。
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