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Paul Goldspink , Ph.D.
Associate Professor
Phone: (414) 456-7575
Email: pgoldspink@mcw.edu

B.Sc. Royal Holloway, London University, 1987
Ph.D. Physiology & Biophysics, University of Illinois at Chicago, 1995.


 

 

Research Interests:

The research in Dr. Goldspink's lab centers around two thematic areas:

1) Improving cardiac muscle contractile function during disease and failure.

2) Enhancing cardiac repair and regeneration using stem cells and biomimicry.Intersecting these two areas of cardiac muscle function and biology is the influence of insulin-like growth factor-1 isoforms and their function.


Summary: Pleiotropy is the phenomenon whereby a single gene has multiple consequences in numerous tissues. IGF-1 exerts pleiotropic effects on numerous tissues by influencing different cellular processes such as proliferation, protein expression, growth and metabolism. The IGF-1 gene gives rise to different isoforms in various tissues during development, in response to hormonal stimulation, nutrition, aging and disease. An underlying hypothesis of this research is the pleiotropic actions of IGF-1 (and the IGF system), are manifest in isoform function. Consequently, we are investigating the role of IGF-1 isoforms in response to stresses such a mechanical overload, hypoxia and oxidative stress in the heart. We have focused on a particular isoform of IGF-1, called Mechano-Growth Factor (MGF), which plays a protective role in preventing cell death, preserving contractility and preventing hypertrophy of the heart following myocardial infarction. We are currently investigating the underlying mechanisms by which this occurs utilizing peptide analogs to examine the functional regions of MGF. In addition, we are examining the regulation of the isoforms to better understand the function biology of the IGF-1 isoforms in general.

This work continues to grow in a number of different directions. We are presently investigating the influence of these IGF-1 isoform peptides on resident cardiac stem/progenitor cells, with a view of using them to enhance cardiac repair. We are exploiting these findings in a number of different ways. We (and collaborators) have developed a technology that combines a microscopic physical scaffold, to provide the physical cues tissue growth combined with the capacity to deliver peptide therapeutics. The goal is to develop a “biomimetic” approach that optimizes stem cell therapy. This approach of implantable cell-sized “biomimetic devices” could serve to instruct cells in order to enhance natural tissue repair and regeneration in other tissues as well as the heart.



Recent Publications:

  • Goldspink PH, Ruch R, Los T, Buttrick PM, García J. Maladaptational changes in Ca2+ homeostasis in cardiac myocytes with age and the onset of hypertrophic stimuli. Pflugers Arch-Eur J Physiol. 456(3):479-87.2008.
  • Shioura KM, Geenen DL, Goldspink PH. Sex related differences in cardiac function during the progression to heart failure following myocardial infarction in mice. Am J Physiol Regul Integr Comp Physiol .5(2):R528-34. 2008.
  • Koshman YE, Waters SB, Walker LA, Los T, de Tombe PP, Goldspink PH, Russell B. A novel method for subcellular delivery and visualization of proteins conjugated to quantum dots. J. Mol Cell Cardiol. 45(6):853-6. 2008.
  • Boateng SY, Senyo SE, Qi L, Goldspink PH, Russell B. Myocyte remodeling in response to hypertrophic stimuli requires nucleocytoplasmic shuttling of muscle LIM protein. J. Mol Cell Cardiol 47(4):426-35. (Editorial 423-425). 2009.
  • Dias FAL, Urboniene D, Yuzhakova M, Pena JR, Goldspink PH, Geenen DL, Wolska BM. Ablation of iNos Delays Cardiac Contraction Dysfunction and Attenuates Hypertrophy Gene Expression Induced by Chronic Pressure Overload. Front Biosci (Elite Ed). Jan 1;2:312-24. 2010.
  • Peña JR, Szkudlarek AC, Warren CM, Heinrich LS, Gaffin RD, Jagatheesan G, Del Monte F, Hajjar RJ, Goldspink PH, Solaro RJ, Wieczorek DF, Wolska BM. Neonatal gene transfer of Serca2a delays onset of hypertrophic remodeling and improves function in familial hypertrophic cardiomyopathy. J Mol Cell Cardiol. 49(6): 993-1002. 2010.
  • Collins JM, Goldspink PH, Russell B. Migration and proliferation of human mesenchymal stem cells is stimulated by different regions of the mechano-growth factor prohormone. J Mol Cell Cardiol. 49(6):1042-5. 2010.
  • Shioura KM, Farjah M, Solaro RJ, Goldspink PH. Myofilament calcium sensitization delays decompensated hypertrophy differently between the sexes following myocardial infarction. Am J Physiol Regul Integr Comp Physiol. 2011 Feb;300(2):R361-8.
  • Gaffin, RD., Peña, JR., Alves, MSL., Dias, FAL., Heinrich, LS., Goldspink, PH., Kranias, EG., Wieczorek, DF., Wolska, BM. Long-term Rescue of a Familial Hypertrophic Cardiomyopathy Caused by a Mutation in the Thin Filament Protein, Tropomyosin, via Modulation of a Calcium Cycling Protein. J Mol Cell Cardiol. Nov; 51(5):812-20. 2011
  • Avner BS., Shioura KM., Scruggs SB., Geenen DL., Helseth DL., Farjah M., Goldspink PH., Solaro RJ. Myocardial Infarction in Mice Alters Sarcomeric Function via Post-Translational Protein Modification. Molecular and Cellular Biochemistry. 2011 Dec 8. In press.


Faculty Collaboration Database - Paul Goldspink, PhD

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