| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4262798 | Transplantation Proceedings | 2007 | 4 Pages |
ObjectiveThe objective of this study was to investigate the role of differentiation growth factor-8 (GDF-8) in inhibiting myofibrosis of abdominal aorta grafts.MethodsMale Spague-Dawley (SD) rats that received abdominal aorta grafts from male Wistar rats were randomly divided into 2 groups: prolonged cold ischemia (PCI) and control groups. Hematoxylin-eosin (HE) staining was performed to examine aortic graft morphology and to measure neointimal thickness. RT-PCR demonstrated the expression of GDF-8. Immunohistochemical staining (IHC) was performed to detect the expression of Smad4, a pivotal molecule of the transforming, growth factor-β (TGF-β)/Smad signal pathway.ResultsThe intimal thickness increased by 14 days following transplantation in the PCI group (P < .05), reaching 381.952 ± 44.334 μm at 28 days, which was higher than that of the control group (56.898 ± 17.543 μm; P < .05). The GDF-8 expression in the PCI group was only 3.6%–33.8% of that among the control group. There was a much higher expression of Smad4 on the endothelium of the PCI than the control group at the same time.ConclusionsProlonged cold ischemia accelerated grafts myofibrosis by down-regulating the expression of GDF-8, which plays a key role in the myofibrosis process of rat abdominal aortic grafts.
