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Myocardial physiology in the aftermath of myocardial infarction (MI) before remodeling is an under-explored area of investigation. Here, we describe the effects of MI on the cardiac sarcomere with focus on the possible contributions of reactive oxygen species. We surgically induced MI in 6–7-month-old female CD1 mice by ligation of the left anterior(More)
This study was performed to elucidate the relation between in vivo measurements of two-dimensional principal strains and the progression of left ventricle (LV) wall thinning during development of dilated cardiomyopathy in the protein kinase C-epsilon (PKC-epsilon) transgenic (TG) overexpressing mouse heart. Principal two-dimensional strains, E1 and E2, were(More)
Insulin-like growth factor I (IGF-1) is an important peptide synthesized in response to growth hormone stimulation. Alternative promoters and an elaborate alternative splicing regulated in a tissue-and developmentally-specific manner result in the production of several distinct isoforms of IGF-1 [reviewed in Gorecki et al. (2007); Matheny et al. (2010)].(More)
Myocardial infarction (MI) is a major cause of heart failure (HF) with the progressive worsening of cardiac performance due to structural and functional alterations. Therefore, we studied cardiac function in adult mice following MI using the Millar pressure-volume (P-V) conductance catheter system in vivo during the later phase of compensatory remodeling(More)
The assembly of sarcomeric proteins into the highly organized structure of the sarcomere is an ordered and complex process involving an array of structural and associated proteins. The sarcomere has shown itself to be considerably more complex than ever envisaged and may be considered one of the most complex macromolecular assemblies in biology. Studies(More)
Protein kinase C (PKC) modulates cardiomyocyte function by phosphorylation of intracellular targets including myofilament proteins. Data generated from studies on in vitro heart preparations indicate that PKC phosphorylation of troponin I (TnI), primarily via PKC-epsilon, may slow the rates of cardiac contraction and relaxation (+dP/dt and -dP/dt). To(More)
Insulin-like growth factor-1 (IGF-1) isoforms are expressed via alternative splicing. Expression of the minor isoform IGF-1Eb [also known as mechano-growth factor (MGF)] is responsive to cell stress. Since IGF-1 isoforms differ in their E-domain regions, we are interested in determining the biological function of the MGF E-domain. To do so, a synthetic(More)
Hypoxia-inducible factor 1α (HIF-1α) plays a role in a number of cell protective pathways following ischemia. There are clear gender related differences in the remodeling process and hearts from males tend to dilate in response to pathologic loads and ischemia to a greater degree than hearts from females. Thus, we hypothesized that there would be a gender(More)
Contractile dysfunction is common to many forms of cardiovascular disease. Approaches directed at enhancing cardiac contractility at the level of the myofilaments during heart failure (HF) may provide a means to improve overall cardiovascular function. We are interested in gender-based differences in cardiac function and the effect of sarcomere activation(More)
Genetic variability has a profound effect on the development of cardiac hypertrophy in response to stress. Consequently, using a variety of inbred mouse strains with known genetic profiles may be powerful models for studying the response to cardiovascular stress. To explore this approach we looked at male C57BL/6J and 129/SvJ mice. Hemodynamic analyses of(More)
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