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The myofibrosis mechanism of differentiation growth factor-8 on rat abdominal aorta grafts
1Department of Burn and Plastic Surgery, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China. chengjingao2003@yahoo.com.cn
Objective:
The objective of this study was to investigate the role of differentiation growth factor-8 (GDF-8) in inhibiting myofibrosis of abdominal aorta grafts.
Methods:
Male 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-beta (TGF-beta)/Smad signal pathway.
Results:
The intimal thickness increased by 14 days following transplantation in the PCI group (P<.05), reaching 381.952+/-44.334 microm at 28 days, which was higher than that of the control group (56.898+/-17.543 microm; 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.
Conclusions:
Prolonged 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.
Insights
Prolonged cold ischemia accelerates abdominal aortic graft myofibrosis by reducing differentiation growth factor-8 (GDF-8) expression. This study highlights GDF-8
Area of Science:
- Vascular surgery
- Regenerative medicine
- Biomedical engineering
Background:
- Abdominal aortic graft complications can arise from myofibrosis.
- Understanding the molecular mechanisms behind graft myofibrosis is crucial for improving outcomes.
Purpose of the Study:
- To investigate the role of differentiation growth factor-8 (GDF-8) in inhibiting abdominal aortic graft myofibrosis.
- To explore the impact of prolonged cold ischemia (PCI) on GDF-8 expression and myofibrosis in aortic grafts.
Main Methods:
- Male Sprague-Dawley rats received abdominal aorta grafts from Wistar rats, divided into PCI and control groups.
- Hematoxylin-eosin staining assessed graft morphology and neointimal thickness.
- RT-PCR and immunohistochemistry detected GDF-8 and Smad4 expression, respectively.
Main Results:
- PCI significantly increased intimal thickness in aortic grafts compared to controls.
- GDF-8 expression was markedly down-regulated in the PCI group.
- Smad4 expression was significantly higher on the endothelium of PCI grafts.
Conclusions:
- Prolonged cold ischemia accelerates graft myofibrosis by down-regulating GDF-8.
- GDF-8 plays a critical role in regulating myofibrosis in rat abdominal aortic grafts.
- Targeting GDF-8 may offer a therapeutic strategy to prevent graft myofibrosis.
