Thrombin peptide (TP508) promotes fracture repair by up-regulating inflammatory mediators, early growth factors, and increasing angiogenesis. Academic Article uri icon

Overview

abstract

  • Previous studies have shown that a single injection of thrombin peptide (TP508) accelerates fracture repair in a closed rat femoral fracture model. The present study was conducted to elucidate the molecular mechanisms of TP508 action using Affymetrix genome-scale profiling and to link early gene expression changes to fracture histology and bone strength changes. Treatment of femoral fractures with TP508 accelerated fracture repair as determined by destructive torsion testing. Blinded histological analysis demonstrated that TP508-treated fracture callus had a significant increase in blood vessels relative to the controls. Gene array analysis showed that TP508 significantly induced expression of early growth factors, inflammatory response modifiers, and angiogenesis-related genes. This study therefore suggests that TP508 promotes fracture repair through a mechanism that involves an increased induction of a number of growth factors, enhanced expression of inflammatory mediators, and angiogenesis-related genes.

publication date

  • December 15, 2004

Research

keywords

  • Fracture Healing
  • Growth Substances
  • Inflammation Mediators
  • Neovascularization, Physiologic
  • Peptide Fragments
  • Thrombin

Identity

Scopus Document Identifier

  • 18244410123

Digital Object Identifier (DOI)

  • 10.1016/j.orthres.2004.10.002

PubMed ID

  • 15885490

Additional Document Info

volume

  • 23

issue

  • 3