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 3
Nuclear accumulation of zyxin is antiapoptotic. TUNEL assay (A) of cultured cardiomyocytes infected with adenoviruses expressing GFP, full-length zyxin (zyxin-w.t.), or nuclear-targeted zyxin for 2 hours followed by treatment with 1 μmol/l staurosporine to induce apoptosis. Results shown were derived from 3 separate experiments. (B) Apoptosis in cultured cardiomyocyte evaluated by DNA laddering. Adenoviruses expressing β-gal or zyxin as wild-type, GFP-conjugated full length (GFP), residues 1-322 (N-term), residues 349–542 (C-term), or NES-deleted residues 322–331 (NES). Apoptotic stimulation was initiated by overexpression of pyk2 kinase as previously described (35). Typical result is shown of 3 separate repetitions for the laddering experiment. (C) TUNEL assay of cultured cardiomyocytes shows protective effect of nuclear-targeted zyxin accumulation in response to apoptotic challenge by ANP (10^–6 M) but lack of protection by ANP (10^–9 M) in response to apoptotic challenge by full-length wild-type zyxin accumulation. Adenoviral vectors were used for expression of zyxin constructs with GFP expression shown as a control for effects of ANP treatments. *P < 0.01; **P < 0.05.