Regulation of Glucose Transporter 1 by Protein Kinase C in Peritoneal Mesothelial Cells Under High Glucose

被引:0
|
作者
Ding, Hong [1 ]
Yin, Li [1 ]
Yang, Qi [1 ]
Che, Yuqin [2 ]
机构
[1] China Med Univ, Affiliated Hosp 4, Div Nephrol, Shenyang 110032, Liaoning Provin, Peoples R China
[2] China Med Univ, Affiliated Hosp 4, Div Neurol, Shenyang 110032, Liaoning Provin, Peoples R China
关键词
Peritoneal Mesothelial Cells; Glucose Transporter 1; Protein Kinase C; Peritoneal Dialysis; EPITHELIAL-MESENCHYMAL TRANSITION; GLUT1; INSULIN; STIMULATION; MEMBRANE; PATHWAYS; FIBROSIS; DIALYSIS;
D O I
10.1166/jbt.2016.1398
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Objective: To investigate the regulation of membrane glucose transporter 1 (GLUT1) by protein kinase C (PKC) in cultured rat peritoneal mesothelial cells (PMCs) under high glucose, and to explore how to avoid peritoneal injury and to improve the efficacy of peritoneal dialysis during long-term peritoneal dialysis. Methods: Peritoneal mesothelial cells (PMCs) were extracted from of male Wistar rats using pancreas enzyme digestion and were cultured cells under different concentrations of glucose and PKC inhibitor Go6976, GLUT1 expression in PMCs was determined with indirect immunofluorescence, the change of GLUT1 expression in the cell membrane before and after each treatment was quantitatively studied with flow cytometry, and change of concentration of glucose in the culture medium was determined by biochemical analyzer. Results: High glucose can induce the expression of GLUT1 in the cell membrane, accompanied by increased glucose transportation by PMCs (P < 0.05). Go6976 significantly inhibited high glucose-induced GLUT1 expression as well as the induced glucose transport. Conclusion: High glucose upregulates GLUT1 expression in the membrane of PMCs in a concentration-dependent manner, accompanied by increased glucose transport by PMCs. PKC mediated pathway plays an important role in this process, and application of PKC inhibitors can antagonize high glucose induced expression of GLUT1.
引用
收藏
页码:61 / 66
页数:6
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