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Title: | Inhibition of Neointima Hyperplasia, Inflammation, and Reactive Oxygen Species in Balloon-Injured Arteries by HVJ Envelope Vector-Mediated Delivery of Superoxide Dismutase Gene |
Authors: | Lin, Shao-Lin Yeh, Jwu-Lai Chang, Tsung-Hsien Huang, Wei-Chun Lee, Song-Tay Wassler, Michael Geng, Yong-Jian Sulistyowati, Erna |
Keywords: | Gene therapy Reactive oxygen species Restenosis Superoxide dismutase |
Issue Date: | 6-Sep-2018 |
Publisher: | Springer |
Series/Report no.: | Translational Stroke Research;Vol.30, Pages 413-427 |
Abstract: | Extracellular superoxide dismutase (EC-SOD) has been implicated in regulation of vascular function but its underlying molecular mechanism is largely unknown. These two-step experiments investigate whether hemagglutinating virus of Japan envelope (HVJ-E) vector-mediated EC-SOD gene delivery might protect against neointima formation, vascular inflammation, and reactive oxygen species (ROS) generation, and also explore cell growth signaling pathways. The first in-vitro experiment was performed to assess the transfection efficacy and safety of HVJ-E compared to lipofectamine®. Results revealed that HVJ-E has higher transfection efficiency and lower cytotoxicity than those of lipofectamine®. Another in-vivo study initially used balloon denudation to rat carotid artery, then delivered EC-SOD cDNA through the vector of HVJ-E. Arterial section with H&E staining from the animals 14 days after balloon injury showed a significant reduction of intima-to-media area ratio in EC-SOD transfected arteries when compared with control (empty vector-transfected arteries) (p < 0.05). Arterial tissue with EC-SOD gene delivery also exhibited lower levels of ROS, as assessed by fluorescent microphotography with dihydroethidium staining. Quantitative RT-PCR revealed that EC-SOD gene delivery significantly diminished mRNA expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1β (p < 0.05 in all comparisons). An immunoblotting assay from vascular smooth muscle cell (VSMC) cultures showed that the EC-SOD transfected group attenuated the activation of MEK1/2, ERK1/2, and Akt signaling significantly. In conclusion, EC-SOD overexpression by HVJ-E vector inhibits neointima hyperplasia, inflammation, and ROS level triggered by balloon injury. The modulation of cell growth-signaling pathways by EC-SOD in VSMCs might play an important role in these inhibitory effects. |
Description: | [ARCHIVES] Copyright Article from: Translational Stroke Research |
URI: | https://link.springer.com/article/10.1007/s12975-018-0660-9 http://repository.unisma.ac.id/handle/123456789/2033 |
Appears in Collections: | LP - Medical Education |
Files in This Item:
File | Description | Size | Format | |
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dr. Erna-5- Lin2019_Article_InhibitionOfNeointimaHyperplas.pdf | Document | 5.59 MB | Adobe PDF | View/Open |
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