Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice
J. Clin. Invest. Daniela Tirziu, et al. 117:3188 doi:10.1172/JCI32024 [Go to this article.]

Figure 7
Angiogenesis-induced hypertrophy in the setting of MI. (A) PR39 induction in tTA⁺/PR39⁺ mice at the time of LAD ligation resulted in reduction of the infarct size 28 days after MI (n = 6 mice/group). (B) Ejection fraction (EF) assessed by pressure-volume loop analysis at 28 days after MI in induced tTA⁺/PR39⁺ and control mice. (C and D) Cross-sectional area of cardiomyocytes in the free (normal) LV wall myocardium in induced tTA⁺/PR39⁺ and control mice expressed as percentage of control. (D) Representative laminin immunostaining of LV myocardium from the 2 mouse groups. (E) Infarct size 28 days after MI in C57BL/6 mice exposed to Ad–hVEGF-B₁₆₇ (black bars) or control virus (Ad-RR5, white bars). Sham, gray bars. Ad–hVEGF-B₁₆₇, n = 16; Ad-RR5, n = 12; sham, n = 5. (F and G) Capillary count (F) and capillary/myocyte ratio (G) in mice exposed to Ad–VEGF-B₁₆₇ or Ad-RR5 28 days after MI or in sham-operated mice. (H and I) Cardiomyocyte hypertrophy in the remote myocardium. Laminin staining (H) and quantitative analysis (I) of cardiomyocyte area in the normal myocardium of C57BL/6 mice 28 days after MI or a sham procedure and exposed to Ad–hVEGF-B₁₆₇ or Ad-RR5. (J) LV function (fractional shortening) 28 days after MI or a sham procedure in C57BL/6 mice exposed to Ad–hVEGF-B₁₆₇ or Ad-RR5. *P < 0.05; **P < 0.05 versus sham. Scale bars: 50 μm.