Alcendor et al. [ 2] demonstrated that moderate overexpression of Sirt1 up to 7.5-fold attenuated age-dependent cardiac dysfunction and oxidative stress-induced apoptosis in mouse hearts, whereas a higher level (12.5-fold) of overexpression of Sirt1 increased apoptosis and hypertrophy and decreased cardiac function.
The authors present data indicating that newt and zebrafish heart muscle cells contain centrosomes, whereas adult mouse heart cells do not.
This also suggests that the two proteins can partially compensate for each other because the disruption of Xin expression in chicken results in abnormal cardiac morphogenesis, whereas the Xinα-null mouse heart still develops normally.
However, this is the first study to demonstrate that pacing a Cx43-deficient mouse heart alters indexes of repolarization and refractoriness, whereas no such changes occur with pacing in the wild-type mouse.
Whereas overexpression of wild-type Twinkle promote recombination of mouse heart mtDNA, mice carrying the Twinkle dup352 364 mutation show a strong mtDNA replication stalling phenotype, similar to the one observed in cultured cells expressing the same mutation [19].
Transgenic expression of DN-Lats2 was used to inhibit endogenous Lats2 in the mouse heart.
Figure 1 Mouse heart MR (left) and fused with 18F-FDG static PET (right).
We have earlier shown that the overexpression of wild-type Twinkle in mouse heart promotes recombination junction formation together with an increase in mtDNA copy number [5] (Figure 4D), whereas the Twinkle dup352 364 mutation has been shown to impair helicase activity, resulting in a strong replication stalling phenotype in cultured cells as well as in mice [19].
Many cells in the HSP60 mouse heart sections were positively labeled by fluorescein-dUTP at the cell nucleus through TUNEL assay, whereas very few TUNEL positively cells were in H+/C− mouse heart sections).
The level of Popdc1 expression in the mouse heart is higher in the atria and cardiac conduction system than in the ventricular working myocardium, whereas Popdc2 is homogeneously expressed throughout the heart, but again with higher levels in the cardiac conduction system [ 6].
