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 1
Effect of lipid lowering on I_KACh and the expression of GIRK1 in cultured embryonic chick atrial myocytes. (A) I-V relationship of the carbachol-induced whole-cell currents elicited from a 1-second voltage ramp with a voltage continuously changing from +50 to –110 mV, from a holding potential of –50 mV (i). Current in a typical atrial myocyte in a high extracellular K⁺ (50 mM), 0 Ca⁺² bath with and without 20 μM carbachol (ii). Current generated by subtracting the trace obtained prior to and after the addition of carbachol (iii). (B) An I-V plot constructed from a series of data points obtained from the carbachol current responses at given voltages. Average carbachol-induced current densities measured in myocytes cultured in FBS or LPDS. Each point is the mean of measurements from 3 independent cultures. (C) Western blot analysis of GIRK1 expression in atrial myocytes cultured in FBS, LPDS, or LPDS supplemented with a mixture of 10 μM cholesterol and 1 μM 25-hydroxycholesterol. (D) Fold stimulation of GIRK1 protein determined by densitometry scanning of 4 independent experiments similar to that in C. Data represent the relative intensity of GIRK1 normalized to β-actin with the value in FBS taken as 1. (E) Fold stimulation of GIRK1 promoter activity above levels in FBS. Data are normalized to β-gal activity and are the mean of 4 independent determinations. *P < 0.05,**P < 0.01 compared with control; ^†P < 0.05 compared with LPDS.