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. 2019 Apr 17;25:101196. doi: 10.1016/j.redox.2019.101196

Fig. 7.

Fig. 7

The AOPPs-induced G1 phase arrest in IEC-6 cells was mediated by RAGE and CD36. IEC-6 cells were pre-incubated with RAGE and CD36 siRNA for 48 h before 200 μg/ml of AOPPs treatment for 120min (b) or 24 h (a, c–e). (a) Flow cytometry results showing a decreased percentage of cells in G1 in response to RAGE and CD36 siRNA in AOPPs-treated cells. Quantitative analyses of FACS data represent percentages of G1 phase cells. (b) Expression levels of phosphorylated and total JNK were detected by Western blotting. The AOPPs-induced activation of JNK was inhibited by RAGE and CD36 siRNA. (c) Representative Western blotting and bar graphs depicting densitometry quantification and showing the increase in cyclin E and CDK2 and decrease in p27kip1 resulting from RAGE and CD36 siRNA treatments in AOPPs-treated cells. (d) Bar graphs representing data acquired from qPCR analysis of cyclin E, CDK2 and p27kip1 mRNA expression in AOPPs-treated IEC-6 cells with RAGE and CD36 siRNA treatments. Relative protein and mRNA levels were normalized with GAPDH, respectively. (e) co-immunoprecipitation analysis results showing that both RAGE and CD36 siRNA suppressed AOPPs-induced interaction of p27kip1 with cyclin E-CDK2 complexes. Data are presented as mean ± SD from three independent experiments; error bars indicate SD. *P < 0.05 and **P < 0.01 versus control; #P < 0.05 and ##P < 0.01 versus AOPPs-treated cells. +CD36 siRNA (2), AOPPs plus CD36 siRNA (2) treatment; +RAGE siRNA (1), AOPPs plus RAGE siRNA (1) treatment.