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. 2009 Mar 16;119(4):976–985. doi: 10.1172/JCI36693

Figure 3. Pmca4b overexpression attenuates stress-induced cardiac hypertrophy.

Figure 3

(A) Aortic pressure gradients across the constriction in control (tTA) and DTG (PMCA4b overexpression) TAC-operated mice. (B) Measurement of heart weight normalized to body weight (HW/BW) in control and DTG mice after 2 weeks of TAC or a sham procedure. *P < 0.05 versus sham, #P < 0.05 versus tTA TAC. (C) Cardiomyocyte surface areas from histological sections of tTA or DTG mice after 2 weeks of TAC normalized to sham surface areas (*P < 0.05 versus sham, #P < 0.05 versus tTA TAC; n = 400 cells from 4–6 hearts). (D) Cardiac fractional shortening in tTA and DTG mice after 2 weeks of TAC or sham procedure. (E) Representative H&E-stained heart sections from tTA and DTG mice after 2 weeks of TAC or a sham procedure. (F) mRNA levels for the indicated genes from hearts of the indicated mice after 4 weeks of TAC. L7 is a control for mRNA content and integrity. Myh7, β-myosin heavy chain; Acta1, skeletal α-actin; Pln, phospholamban. (G) Quantitative analysis of fibrosis area in hearts of the indicated groups 8 weeks after TAC or a sham procedure (*P < 0.05 versus sham, #P < 0.05 versus tTA TAC). (H) Heart weight normalized to body weight in control and DTG mice after 2 weeks of Ang/PE infusion or PBS vehicle treatment. *P < 0.05 versus PBS, #P < 0.05 versus tTA Ang/PE). The number of mice used is shown within the bars of the various graphs.