Research Article

Association between TLR4 and PTEN Involved in LPS-TLR4 Signaling Response

Figure 4

PTEN upregulates NF-κB-dependent gene transcription in RAW264.7 macrophages ( (a), (b)). (a) RAW264.7 cells were transfected by Lipofectamine 2000 with 0.8 μg NF-κB-Luc plasmid and 16 ng of pRL-CMV-Renilla-luciferase plasmid. Twenty-four hours later, the transfected cells were cultured with or without bpV(Pic) 100 nM for 1 hour, followed by the stimulation of LPS (1 μg/mL) for another 6 hours. (b) RAW264.7 cells were transfected by Lipofectamine 2000 with 0.8 μg CMV/wild-PTEN/G129E-PTEN/C124A-PTEN, 0.2 μg NF-κB-Luc plasmid, and 4 ng of pRL-CMV-Renilla-luciferase plasmid. Twenty-four hours later, the transfected cells were left untreated or treated with LPS (1 μg/mL) for 6 hours. Luciferase activities were measured using Dual-Luciferase Reporter Assay System according to the manufactures’ instructions. Data are presented as the relative fold increase in LPS stimulated sample readout over nonstimulated sample readout and are expressed as the mean ± SD. Compared with the bpV(−) group, PTEN inhibitor decreased LPS-induced NF-κB activation significantly () (a). Compared with the empty vector group, overexpressed PTEN enhanced LPS-induced NF-κB activation significantly (). No significant effect was found in mutant PTEN groups and empty vector group (b). and versus LPS (−) group. versus bpv(Pic) (−) group. versus empty vector group.
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