Paul H. Goldspink

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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)
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)
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)
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)
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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