Parasympathetic response in chick myocytes and mouse heart is controlled by SREBP
J. Clin. Invest. Ho-Jin Park, et al. 118:259 doi:10.1172/JCI32011 [Go to this article.]

Figure 4
DN–SREBP-1 blocks the effect of LPDS on GIRK1 expression and I_KACh. (A) DN–SREBP-1 reverses the LPDS-mediated increase in GIRK1 promoter activity. Reporter assays were carried out in atrial myocytes cultured in FBS or LPDS and transfected with GIRK1-Luc plus a plasmid expressing either β-gal or SREBP-1c. Data are the mean of 4 experiments carried out in triplicate. **P < 0.01 compared with FBS; *P < 0.05 compared with LPDS. (B) DN–SREBP-1 blocks the LPDS-mediated increase in GIRK1 protein levels, while having no effect on GIRK1 expression in cells cultured in FBS. Embryonic chick atrial myocytes were infected with an adenoviral vector expressing GFP plus DN–SREBP-1 or GFP plus β-gal at the time of plating (MOI of 20) as described in Methods. On the third culture day, cells were harvested and expression of GIRK1 determined by Western blot analysis. Fluorescence microscopy demonstrated that 80%–90% of cells were GFP positive. (C) Densitometry scanning of 4 experiments similar to that in B. Data are normalized to the expression of Gβ. **P < 0.01 compared with FBS; *P < 0.05 compared with LPDS. (D) Effect of DN–SREBP-1 on I_KACh in cells cultured in LPDS. Embryonic atrial myocytes were cultured in LPDS cells infected with adenovirus expressing GFP plus DN–SREBP-1 or β-gal. I_KACh was determined as described in Figure 1A and the I-V relationship plotted. Points are the mean of 7 determinations in 3 independent cultures. The decrease in current density was significant; P < 0.03.