[Frontiers in Bioscience E4, 2022-2028, January 1, 2012]

TGF-beta 1/Smad3 expression and its effects on carotid intimal hyperplasia

Ping Lu1, Songhao Wang1, Wenwei Cai1, Jing Sheng1

1Department of Geriatrics, Shanghai Ninth People's Hospital Affiliated Shanghai Jiao Tong University School of Medicine, China

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Materials and methods
3.1. Materials
3.2. Establishment of an animal model for each group and sample collection
3.3. Examination of TFG-β1 in serum
3.4. Pathological examination
3.5. Quantitative real-time polymerase chain reaction (PCR)
3.6. Immunohistochemistry
3.7. Statistical Analysis
4. Results
4.1. TGF-beta 1/smad3 expression after vascular injury
4.2. NIH after vascular injury
4.3. In vivo Smad3 expression in vessels after transduction of the antisense adenovirus of smad3
4.4. Effect of the antisense adenovirus of Smad3 on neointimal hyperplasia in vivo
4.5. Expression of Ki-67 in blood vessels
5. Discussion
6. Acknowledgements
7. References

1. ABSTRACT

We investigated expression of TGF-beta 1/Smad3 after balloon injury in rat carotid arteries as well as the effects of blocking the TGF-beta 1/smad3 signaling pathway on carotid intimal hyperplasia. Rats were randomly divided into control group (C group) and injury group (S group). The latter were randomly divided into intervention group (antisense Smad3 adenovirus vector transfection after balloon injury) and blank control group (blank adenovirus vector transfection after balloon injury). Expression of Smad3 mRNA 1 d, 3 d, 1 week, 2 weeks and 1 month after injury and intima/media thickness ratios 1 d, 2 weeks and 3 months after injury in the intervention group were significantly lower than those in the injury group. Ki-67 expression in the intervention group was inhibited as shown in immunohistochemistry studies. These results demonstrated that antisense Smad3 adenovirus vector transfection can block TGF-beta 1/Smad3 signal transduction and thus inhibit intimal hyperplasia.