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Very low density lipoprotein receptor (VLDLR) is thought to participate in the patho- genesis of atherosclerosis induced by VLDL and β-VLDL. The present study was undertaken to elu- cidate the effects of VLDL and β-VLDL on VLDLR expression and its signaling pathway. RAW264.7 cells were incubated with VLDL and β-VLDL. The expression of VLDLR mRNA was detected by RT-PCR. The transcriptional activity of VLDLR gene was detected in recombinant plasmid pGL4.2VR-luciferase transfected RAW264.7. Western blot assay was used to detect the changes of phosphorylated ERK1/2 protein. Inhibitors or activators were used to observe the signal pathway in- volving VLDLR expression regulation. The results showed that VLDL and β-VLDL stimulated ERK1/2 activity in a PKC-dependent manner. VLDL or β-VLDL-induced VLDLR expression on macrophages was extremely abolished by inhibitors ERK1/2 or PKC. Our findings revealed that VLDL or β-VLDL-induced VLDLR expression via PKC/ERK cascades and the effect was linked to the transcriptional activation of VLDLR gene promoter.
Very low density lipoprotein receptor (VLDLR) is thought to participate in the patho- genesis of atherosclerosis induced by VLDL and β-VLDL. The present study was undertaken to elucidate the effects of VLDL and β-VLDL on VLDLR expression and its signaling The expression of VLDLR mRNA was detected by RT-PCR. The transcriptional activity of VLDLR gene was detected in the recombinant plasmid pGL4.2VR-luciferase transfected RAW264.7. Western blot Inhibitors or activators were used to observe the signal pathway-volving VLDLR expression regulation. The results showed that VLDL and β-VLDL stimulated ERK1 / 2 activity in a PKC-dependent manner. VLDL or β-VLDL-induced VLDLR expression on macrophages was extremely abolished by inhibitors ERK1 / 2 or PKC. Our findings revealed that VLDL or β-VLDL-induced VLDLR expression via PKC / ERK cascades and the effect was li nked to the transcriptional activation of VLDLR gene promoter.