Acceleration of soft tissue repair by a thrombin-derived oligopeptide.

Abstract

Augmentation of thrombin-modulated chemotaxis and mitogenic activity within the early phase of soft tissue repair is now possible. Identification of high-affinity thrombin receptor binding domains within thrombin has enabled the synthesis of a family of peptides which interact with thrombin receptors and enhance in vitro mitogenesis. A single (5.0 micrograms/wound) application of the thrombin receptor-activating peptide (P517-30) significantly increased wound breaking strength from Day 5 (31% over controls) to Day 12. Two models of impaired healing created by radiotherapy (RT) were used to elucidate possible mechanisms of P517-30 action. Although P517-30 did not completely overcome the RT-induced healing impairments, it increased breaking strength under conditions of penetrating whole body RT-induced pancytopenia by 22% and of nonpenetrating surface RT-induced dermal cell damage by 42%. This suggests that P517-30 directly stimulates resident endothelial cells, fibroblasts, or other cells to overcome dermal and circulating monocytic deficits. These results suggest a method to accelerate wound healing with potential clinical applications and emphasize the activity of thrombin as a growth factor.

• Authors: D T Cromack, B H Porras-Reyes, S S Wee, K C Glenn, J A Purdy, D H Carney, T A Mustoe
• Journal: The Journal of surgical research (J Surg Res) Vol. 53 Issue 2 Pg. 117-22 (Aug 1992) ISSN: 0022-4804 [Print] United States
• PMID: 1405599 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Peptide Fragments
• thrombin receptor-activating peptide (P508-530)

Topics

• Amino Acid Sequence
• Animals
• Male
• Molecular Sequence Data
• Peptide Fragments (pharmacology)
• Rats
• Rats, Wistar
• Time Factors
• Wound Healing (drug effects, radiation effects)