Atrial natriuretic peptide promotes cardiomyocyte survival by cGMP-dependent nuclear accumulation of zyxin and Akt
J. Clin. Invest. Takahiro Kato, et al. 115:2716 doi:10.1172/JCI24280 [Go to this article.]

Figure 5
Nuclear accumulation of zyxin is mediated by cGMP-dependent signaling. Time course of zyxin nuclear accumulation in cultured cardiomyocytes treated with cGMP (10^–4 M). (A) Confocal microscopy shows distribution of zyxin (green in overlay) and myofibrils (red in overlay) following exposure to cGMP. Cells were labeled with phalloidin (actin filament) to reveal sarcomeric organization. Scale bars: 30 μm. (B) Time course of nuclear zyxin accumulation shows peak level within minutes after treatment and return to normal level within 3 hours. (C) Activation of PKA or PKC signaling did not induce zyxin nuclear translocation. Bar graph shows the ratio of zyxin nuclear translocation with cGMP (10^–4 M), PMA (10 ng/ml), or forskolin (10–⁵ M) treatment for 1 hour as assessed by confocal microscopy. (D) Participation of ANP or PKG in nuclear translocation of zyxin was demonstrated by use of HS142-1 (ANP receptor inhibitor; 10 μg/ml) or KT5823 (PKG inhibitor; 5 × 10^–6 M). Bar graph shows the ratio of zyxin nuclear translocation with or without inhibitor pretreatment followed by stimulation with cGMP (10^–4 M) or ANP (10^–9 M). n = 3 for all experiments.