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. Author manuscript; available in PMC: 2012 Aug 5.
Published in final edited form as: Circ Res. 2011 Jun 23;109(4):407–417. doi: 10.1161/CIRCRESAHA.110.228452

Figure 4. Calcineurin-induced ventricular hypertrophy precedes systolic dysfunction, and fetal gene activation is delayed after calcineurin activation.

Figure 4

Figure 4

Figure 4

A: Mean LV mass calculated from serial 2D echocardiographic images of tTA (n=9) and tTA/CnA* (n=9) mice recorded after removing doxycycline. B: Mean LV posterior wall thickness at end-diastole (LVPWd) by serial echocardiography after removing doxycycline. C: Mean percent fractional shortening from serial M-mode tracings obtained after removing doxycycline. D: Mean LV internal diameter in diastole (LVIDd) measured from serial 2D echocardiographic images obtained after removing doxycycline. E,F: Quantitative real-time RT-PCR measurements of mRNA levels of indicated genes from RNA isolated from selected hearts at (E) one week and (F) eight weeks after removing doxycycline. mRNA levels are calculated relative to cyclophilin mRNA and normalized to control levels. *p < 0.01. ON: double-transgenic tTA/CNA mice; OFF: single transgenic tTA mice.