Gerald M Fuller

Publications (2)1.75 Total impact

• Source

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  Chapter: Thrombin and Thrombin Peptides in Wound Healing and Tissue Repair

  Barbara Olszewska-Pazdrak, John S. Bergmann, Gerald M. Fuller, Darrell H. Carney
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  ABSTRACT: Thrombin and thrombin peptides play a key role in wound healing and tissue regeneration. Early events initiated by thrombin contribute to inflammatory cell recruitment and activation of inflammatory cells. Certain nonproteolytic effects of thrombin, or thrombin peptides presumably released from fibrin clots, also appear to affect revascularization and progression of the repair process. Thus, the role of thrombin in wound healing goes far beyond hemostasis. Recent animal studies and human clinical trials with TP508, a specific 23 amino acid peptide representing a receptor-binding domain of thrombin, show significant improvement in healing and revascularization of dermal wounds and bone fractures. These studies highlight a role of thrombin peptides in wound healing that is just beginning to be recognized.
  04/2010: pages 115-132;
• Article: TP508 (Chrysalin) reverses endothelial dysfunction and increases perfusion and myocardial function in hearts with chronic ischemia.

  Theresa W Fossum, Barbara Olszewska-Pazdrak, Michelle M Mertens, Lori A Makarski, Matthew W Miller, Travis W Hein, Lih Kuo, Fred Clubb, Gerald M Fuller, Darrell H Carney
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  ABSTRACT: Endothelial dysfunction (ED) is characterized by impaired nitric oxide (NO) signaling, decreased NO-dependent vasodilatation, increased vascular inflammation, and diminished response to angiogenic factors. TP508 (Chrysalin), an angiogenic tissue repair peptide, was tested for potential effects on myocardial revascularization and ED using a porcine model of chronic myocardial ischemia. TP508 increased perfusion in ischemic regions up to16-fold (P < .02) and doubled myocardial wall thickening (P < .02) relative to placebo controls. Ischemic arterioles exhibited impaired NO-mediated vasodilation and diminished NO production. TP508 reversed ischemic effects, increasing NO-mediated vasodilation (P < .05), endothelial nitric oxide synthase (eNOS) expression, and NO production. In human endothelial cells, TP508 stimulated eNOS activation (1.84 +/- 0.2-fold; P < .02), increased NO production (85 +/- 18%; P < .02), and prevented hypoxia-induced eNOS downregulation (P < .01). Thus, TP508 reverses ED both in porcine ischemic hearts and cultured human endothelial cells. These results suggest potential therapeutic benefit of TP508 in myocardial revascularization and treatment of ED-related diseases.
  Journal of Cardiovascular Pharmacology and Therapeutics 10/2008; 13(3):214-25. · 1.75 Impact Factor