Pressure-independent cardiac hypertrophy in mice with cardiomyocyte-restricted inactivation of the atrial natriuretic peptide receptor guanylyl cyclase-A
J. Clin. Invest. Rita Holtwick, et al. 111:1399 doi:10.1172/JCI17061 [Go to this article.]

Figure 2
Demonstration of the GC-A deletion at the mRNA and protein level. (a) RT-PCR analyses of GC-A and GAPDH mRNA in preparations of isolated adult ventricular cardiomyocytes from floxed GC-A and CM GC-A KO mice (20–30 single cells were collected from each heart; five hearts were studied per genotype). Left: Ethidium bromide visualization of RT-PCR products. Left ventricle (LV) of a floxed GC-A mouse was used as positive control. Right: GC-A signal intensities were normalized to GAPDH. (b) Basal and ANP-stimulated guanylyl cyclase activity of plasma membranes isolated from whole hearts of floxed GC-A and CM GC-A KO mice. Enzymatic activity is expressed as picomoles of cGMP formed per milligram of protein over 10 minutes (n = 6). *P < 0.05 vs. floxed GC-A.