Regulation of p38 MAPK, HSP27 and ERK1/2 phosphorylations by WDR12.

<p><b>A.</b> and <b>B.</b> p38 MAPK and HSP27 phosphorylations were up-regulated in normal heart, <b>D.</b> and <b>E.</b> after infarction, and <b>G.</b> and <b>H.</b> p38 MAPK in Ang II-induced hypertension at 1 week after WDR12 gene delivery. <b>C.</b> ERK1/2 phosphorylations were up-regulated in normal heart at 3 days, and <b>I</b>. in Ang II-induced hypertension at 1 week, but not post-infarction <b>(F)</b>. <b>J. K.</b> and <b>L.</b> p38 MAPK, HSP27 and ERK1/2 phosphorylations were increased by adenoviral transfection of WDR12 <i>in vitro</i> in rat neonatal cardiomyocytes (n = 7 to 10). <b>A-C.</b> open bars represent LacZ and solid bars WDR12. *<i>P</i><0.05, **<i>P</i><0.01, ***P<0.001 versus LacZ-control group (Student <i>t</i> test). <b>M. N.</b> and <b>O.</b> p38 MAPK, HSP27 and ERK1/2 phosphorylations were decreased by WDR12 siRNA transfection <i>in vitro</i> in rat neonatal cardiomyocytes (n = 4). *<i>P</i><0.05 versus negative control group (1-way ANOVA followed by LSD post hoc test). The results are mean±SEM. Representative Western blots are shown. Bands were detected from the same gel.