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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)
Stem cell function is thought to be tightly regulated by growth factor concentration in the confines of the microenvironmental niche. Therefore, the response of human mesenchymal stem cells (hMSCs) was studied in culture with mechano-growth factor (MGF), an isoform of IGF-1 known to be expressed in the heart following injury. Chemotactic migration of hMSCs(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)
BACKGROUND Mechano-growth factor (MGF) is a splice-variant of IGF-I sharing an identical mature region, but with a different E domain. Our objective was to determine if MGF would reduce the area of 'at-risk' myocardium and improve cardiac function in the post-infarct heart. METHODS Infarcts were induced by injection of microspheres. In experiment 1, sheep(More)
We report characterization of a transgenic mouse that overexpresses constitutively active protein kinase Cepsilon in the heart and slowly develops a dilated cardiomyopathy with failure. The hemodynamic, mechanical, and biochemical properties of these hearts demonstrate a series of temporal events that mark the progression of the disease. In the 3-month(More)
CSRP3 or muscle LIM protein (MLP) is a nucleocytoplasmic shuttling protein and a mechanosensor in cardiac myocytes. MLP regulation and function was studied in cultured neonatal rat myocytes treated with pharmacological or mechanical stimuli. Either verapamil or BDM decreased nuclear MLP while phenylephrine and cyclic strain increased it. These results(More)
Human studies reveal sex differences in myocardial function as well as in the incidence and manifestation of heart disease. Myocellular Ca(2+) cycling regulates normal contractile function; whereas cardiac dysfunction in heart failure has been associated with alterations in Ca(2+)-handling proteins. Beta-adrenergic receptor (beta-AR) signaling regulates(More)
The design of a novel transduction complex has permitted the introduction of protein-quantum dot conjugates into the cytoplasm of living cells. Appropriate subcellular localization of quantum dot-conjugated cardiac troponin C to the myofibrils and a nuclear peptide to the nucleus was attained in living cardiac myocytes using this approach. This new(More)