Chang et al. 10.1073/pnas.0605635103. |
Fig. 6. Twelve pairs of transgenic and non-transgenic (NTg) littermates, ages range from 4-wk, 15-wk, 6-mo, 1-yr, and 2-yr, were examined for heart-weight to body-weight (HtW/BW) ratio to assess sign of cardiac hypertrophy. There is a slight but statistically significant increase in HtW/BW ratio in transgenic animals over the age of 4 mo. Moreover, these older transgenic animals harbored morphologically larger hearts.
Fig. 7. Although the increased heart-weight to body-weight raio in transgenic animals is statistically significant and may indicate cardiac hypertrophy, possibly due to exogenous up-regulation of SMC contractile filaments, careful histological examination should elucidate other pathophysiological conditions such as cardiac dilation or fibrosis. Cardiac samples were harvested from transgenic and non-transgenic littermates and age-matched C57 wild type mouse of 6 mo old, the starting age of increased HtW/BW ratio. Coronal sections of the heart, showing all four chambers, were subject to Masson's trichrome staining, which stains muscle cytoplasm red, collagen green, and nucleus blue. No chamber dilation or increase in ventricular wall thickness were found in three transgenic animals examined. The cardiomyocytes of a MHC-CRP2 mice were homogenous in size and not much larger than those of nontransgenic animals (data not shown). Furthermore, Masson's trichrome staining did not revealed any sign of interstitial fibrosis in the heart of transgenic mouse.
Fig. 8. We know that the CRP2 transgenic mice are alive and show no sign of cardiomyopathy. Yet cardiac-specific misexpression of CRP2 causes exogenous up-regulation of SMC contractile filaments including SM-MHC, in adult hearts. Initial noninvasive functional analysis of 12 transgenic and 10 nontransgenic littermates, using doppler echocardiography, revealed no difference in aortic outflow and cardiac contraction and relaxation, all performed under resting state.