作者机构：
[刘志国] Department of Biotechnology and Chemical Engineering, Wuhan Polytechnic University, Wuhan 430023, China;[赵则春] College of Life Science, Wuhan University, Wuhan 430072, China;[屈伸; 冯友梅; 王燕; 吴凡; 宗义强] Department of Biochemistry and Molecular Biology, Tongji Medical College, Huashong University of Science and Technology, Wuhan 430030
通讯机构：
Department of Biotechnology and Chemical Engineering, Wuhan Polytechnic University, China
摘要：
To explore the intracellular signal pathways for β-VLDL induced very low density lipoprotein receptor (VLDL-R) transcription up-regulation and their effects on lipid accumulation in macrophages, Western Blot was used to examine phosphorylated ERK1/2 protein and regulated effects by different singal kinase inhibitants. It was found that β-VLDL induced an increase in ERK1/2 activity in a protein kinase C (PKC)-dependent manner in murine RAW264.7 macrophages. By using different protein kinases inhibitors or activators, it was observed that the effect of β-VLDL induced VLDL receptor transcription, which was monitored by RT-PCR analysis of VLDL receptor mRNA, was not affected by the inhibitor of p38 kinase and cAMP analog, but extremely abolished by pretreating cells with PD98059, an inhibitor of ERK and GF 109203X, an inhibitor of PKC. These results demonstrated that the PKC-ERK1/2 cascade is the essential signaling pathway by which β-VLDL activated VLDL-R mRNA expression. Inhibition of the ERK1/2 signaling cascade resulted in suppression of the cellular lipid accumulation induced by β-VLDL in macrophages.
