Fig. 7

HDAC2 was involved in the regulation of Sin3A- or MeCP2-suppressed AP-1 transcriptional activity in ET-1-treated WI-38 cells. A Cells were transfected with HDAC2-HA (1 μg), AP-1-luciferase plasmid (1 μg), or pBK-CMV-Lac Z (0.1 μg) for 24 h and then stimulated with ET-1 for 16 h. Bars indicate values of mean ± SEM (n = 5). *p < 0.05 versus ET-1 stimulation. B Cells were transfected with AP-1-luciferase plasmid (1 μg) and pBK-CMV-Lac Z (0.1 μg) and then transfected with Sin3A-HA (0.5 μg) or co-transfected with Sin3A-HA (0.5 μg) and HDAC2 siRNA (100 nM) for 24 h. Cells were stimulated with ET-1 for 16 h. Luciferase activity was evaluated as described in “Materials and methods”. Bars indicate values of mean ± SEM (n = 5). *p < 0.05 versus ET-1-treated cells, ^#p < 0.05 versus Sin3A-transfected cells with ET-1 stimulation. C Cells were transfected with AP-1-luciferase plasmid (1 μg) and pBK-CMV-Lac Z (0.1 μg) and then transfected with MeCP2-HA (0.5 μg) or co-transfected with MeCP2-HA (0.5 μg) and HDAC2 siRNA (100 nM) for 24 h. Cells were stimulated with ET-1 for 16 h. Luciferase activity was evaluated as described in “Materials and methods”. Bars indicate values of mean ± SEM (n = 5). *p < 0.05 versus ET-1-treated cells, ^#p < 0.05 versus MeCP2-transfected cells with ET-1 stimulation