Interestingly, there is an upregulated expression of mXinβ at both message and protein levels in mXinα-null mouse hearts, suggesting mXinβ may be partially compensating for the loss of mXinα [5].
However, chromatin immunoprecipitation revealed reduced RNA polymerase II (Pol II) occupancy at the miR-1-1/miR-133a-2, and miR-1-2/miR-133a-1 promoters in P2 miR-1 double-knockout mouse hearts, suggesting that transcriptional initiation of these loci is reduced secondary to loss of miR-1 expression.
However, individual peptide quantification by GELSILOX of the same data revealed an increase in the proportion of peptides containing oxidized Cys detected in mitochondrial VDAC and a concomitant reduction in the same peptides containing the reduced Cys form in both subsarcolemmal (SSM) and IFM from old mouse hearts, suggesting that aging induces oxidative damage in this protein.
These results demonstrate that not only RCAN1.4 is expressed in hearts, but also its expression is differentially regulated, at least during mouse heart development, suggesting that the expression level of RCAN1.4 might contribute to human CHD.
Our results indicate that acute inflammation stimulates the regenerative response in neonatal mouse heart, and suggest that modulation of inflammatory signals might have important implications in cardiac regenerative medicine.
For example, identification of rac1 in the Drosophila heart suggests that it may provide a valuable model to complement mouse studies of rac1-mediated hypertrophy [34], [35].
The intravenous administration of lipopolysaccharide into mice induces expression in the kidney and heart, suggesting that ADAMTS-1 is an inflammation-associated gene product [ 4].
Hibernation has been described in the septic mouse heart [32] and suggested in human critical illness [33, 34].
PDE4 localizes to the Z-band of cardiomyocytes in human (Fig. 1c) and mouse heart (data not shown), suggesting that PDE4 activity detected in heart extracts is due to the expression of PDE4 in the cardiomyocytes and that PDE4 acts in defined subcellular compartments of these cells.
In a recent study, we showed that the EphA6-R localizes to the vasculature and increased in response to injury in EphA2-R-M mouse hearts [ 76], suggesting that EphA6-R compensates for the absence of EphA2-R.
