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| dc.contributor.author | Lin, Shao-Lin | |
| dc.contributor.author | Yeh, Jwu-Lai | |
| dc.contributor.author | Chang, Tsung-Hsien | |
| dc.contributor.author | Huang, Wei-Chun | |
| dc.contributor.author | Lee, Song-Tay | |
| dc.contributor.author | Wassler, Michael | |
| dc.contributor.author | Geng, Yong-Jian | |
| dc.contributor.author | Sulistyowati, Erna | |
| dc.date.accessioned | 2021-10-14T01:45:01Z | |
| dc.date.available | 2021-10-14T01:45:01Z | |
| dc.date.issued | 2018-09-06 | |
| dc.identifier.uri | https://link.springer.com/article/10.1007/s12975-018-0660-9 | |
| dc.identifier.uri | http://repository.unisma.ac.id/handle/123456789/2033 | |
| dc.description | [ARCHIVES] Copyright Article from: Translational Stroke Research | en_US |
| dc.description.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. | en_US |
| dc.language.iso | en | en_US |
| dc.publisher | Springer | en_US |
| dc.relation.ispartofseries | Translational Stroke Research;Vol.30, Pages 413-427 | |
| dc.subject | Gene therapy | en_US |
| dc.subject | Reactive oxygen species | en_US |
| dc.subject | Restenosis | en_US |
| dc.subject | Superoxide dismutase | en_US |
| dc.title | Inhibition of Neointima Hyperplasia, Inflammation, and Reactive Oxygen Species in Balloon-Injured Arteries by HVJ Envelope Vector-Mediated Delivery of Superoxide Dismutase Gene | en_US |
| dc.type | Article | en_US |
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