Lastly, in vivo imaging studies revealed minimal differences between rosiglitazone-treated and untreated db/db mouse hearts, indicating that rosiglitazone's effects on gene expression in the heart do not immediately turn into detectable gross functional changes.
Similar results were found with synthetic Tat was added on mitochondria isolated from mice heart, indicating that Tat-induced mitochondrial swelling is not restricted to liver mitochondria, and suggesting a common PTP-independent mechanism.
The health of the MRL mouse hearts indicates the opposite may be true and increased reliance upon lipid metabolism is the healthy adaptation.
Cardiac hypertrophy, survival, and alternative splicing of CELF targets were all rescued by crossing MHC-CELFΔ mice to mice over-expressing CELF1 in the heart, indicating that both the molecular and gross phenotypes can be attributed to loss of CELF activity [21].
High uptake of ligand in both WT and KO mice within the heart indicated that [C]TGN-020 has some affinity to aquaporin 1 (AQP1), which is shown to have approximately 60% homology with AQP4.
On the other hand, sequences similar to 15,630 mouse UniGenes not known to be expressed in the mouse heart were detected, indicating that the expression information in public databases may be very incomplete.
These results demonstrate that disruption of the titin reading frame due to a truncating DCM mutation can be restored by exon skipping in both patient cardiomyocytes in vitro and mouse heart in vivo, indicating RNA-based strategies as a potential treatment option for DCM.
The present study provides the first proof-of-principle evidence that disruption of the titin reading frame due to a truncating DCM mutation can be restored by exon skipping in both patient cardiomyocytes in vitro and mouse heart in vivo, indicating RNA-based strategies as a potential treatment option for DCM.
This is in accordance with results from SAGE analysis of the adult mouse heart transcriptome, which indicate that the cardiac tissue contains the highest percentage of mitochondrial-genome derived transcripts [ 37, 38].
As shown by quantitative Taqman-PCR with specific CTGF mouse and rat primers and probes, the endogenous CTGF expression was strongly induced in CTGF-TG mouse hearts (Figure 1D) indicating an autocrine mechanism driving the CTGF expression in the heart.
