In contrast, the IFM isolated from younger mice heart demonstrated significantly higher OCR in response to succinate or ascorbate/TMPD compared to IFM isolated from older mice heart (Fig. 5B D).
Immunoblot analysis of O-GlcNAc-modified proteins in MuRF3−/− hearts demonstrated no differences from wildtype hearts when mice were fed a chow diet or 26 weeks of high fat diet (Additional file 2: Figure S2).
In situ hybridization on histological sections of embryonic hearts demonstrated reduced Shox2 expression in the IFT of the Tbx5del/+ mutant mice at E11.5 (Fig. 3Ca and b).
In a fourth experiment on mitochondria isolated from live mouse hearts, the authors demonstrated that administering Zn2+ resulted in rapid mitochondrial swelling, another indication of a loss of mitochondrial function.
By measuring intracellular calcium, developed pressures and myocardial oxygen consumption in perfused mouse hearts, these results demonstrate that high perfusate calcium positive inotropy compared to dobutamine results in reduced myofilament responsiveness to intracellular calcium, which is associated with energetic inefficiency and evidence of protein kinase C activation.
Accordingly, forced expressions of MEF2A, C and D in mice heart were demonstrated to be sufficient to drive intolerance to pressure overload, ventricular chamber dilation and contractile dysfunction[8], [9], [10].
Loss of the mammalian CDKI, p27Kip1, in mice leads to bigger organs, including the heart, demonstrated to be due to an increase in the total cell number.
Recent work has demonstrated that neonatal mouse hearts have a regenerative capacity similar to zebrafish during the first 7 days after birth (P1-7); however, following P7 this capacity for heart renewal declines dramatically [126].
Hypokalaemic mouse hearts recapitulate the clinical arrhythmogenic phenotype, demonstrating EADs and triggered beats that might initiate VT on the one hand and reduced transmural dispersion of repolarization reflected in ΔAPD90 suggesting arrhythmogenic substrate on the other.
More recently, we demonstrated that DUSP4-/ mouse hearts suffer greater infarct than wild-type (WT) and have poor post-ischemic functional recovery when subjected to ischemia/reperfusion (I/R) injury.
