1,721,115 research outputs found
Loss of cardiac mass and function induced by 17beta-oestradiol via a beta-catenin mechanism in C57Bl/6N female mice
No full textCyclinD2-overexpression augment the afterload induced hypertrophic response and improves the survival
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Administration of 17 beta-Estradiol in C57Bl/6N Female Mice Leads to Cardiac Atrophy and Dysfunction via a beta-Catenin Mechanism
No full textDual-Specificity Tyrosine Phosphorylation-Regulated Kinase 1A is a NFAT Kinase Mediating Negative Feedback on Calcineurin/NFAT Signaling.
No full textCell Cycle-Mediated Cardiac Regeneration in the Mouse Heart
No full textMany forms of heart disease result in the essentially irreversible loss of cardiomyocytes. The ability to promote cardiomyocyte renewal may be a promising approach to reverse injury in diseased hearts. PURPOSE OF REVIEW: To describe the impact of cardiomyocyte cell cycle activation on cardiac function and structure in several different models of myocardial disease. RECENT FINDINGS: Transgenic mice expressing cyclin D2 (D2 mice) exhibit sustained cardiomyocyte renewal in the adult heart. Earlier studies demonstrated that D2 mice exhibited progressive myocardial regeneration in experimental models of myocardial infarction, and that cardiac function was normalized to values seen in sham operated litter mates by 180 days post-injury. D2 mice also exhibited markedly improved atrial structure in a genetic model of atrial fibrosis. More recent studies revealed that D2 mice were remarkably resistant to heart failure induced by chronic elevated afterload as compared to their wild type (WT siblings), with a 6-fold increase in median survival as well as retention of relatively normal cardiac function. Finally, D2 mice exhibited a progressive recovery in cardiac function to normal levels and a concomitant reduction in adverse myocardial remodeling in an anthracycline cardiotoxicity model. SUMMARY: The studies reviewed here make a strong case for the potential utility of inducing cardiomyocyte renewal as a means to treat injured hearts. Several challenges which must be met to develop a viable therapeutic intervention based on these observations are discussed
X-Ray Structural Analysis of Single Adult Cardiomyocytes: Tomographic Imaging and Microdiffraction
No full textWe present a multiscale imaging approach to characterize the structure of isolated adult murine cardiomyocytes based on a combination of full-field three-dimensional coherent x-ray imaging and scanning x-ray diffraction. Using these modalities, we probe the structure from the molecular to the cellular scale. Holographic projection images on freeze-dried cells have been recorded using highly coherent and divergent x-ray waveguide radiation. Phase retrieval and tomographic reconstruction then yield the three-dimensional electron density distribution with a voxel size below 50 nm. In the reconstruction volume, myofibrils, sarcomeric organization, and mitochondria can be visualized and quantified within a single cell without sectioning. Next, we use microfocusing optics by compound refractive lenses to probe the diffraction signal of the actomyosin lattice. Comparison between recordings of chemically fixed and untreated, living cells indicate that the characteristic lattice distances shrink by ∼10% upon fixation
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