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dc.contributor.authorLin, Shao-Lin
dc.contributor.authorYeh, Jwu-Lai
dc.contributor.authorChang, Tsung-Hsien
dc.contributor.authorHuang, Wei-Chun
dc.contributor.authorLee, Song-Tay
dc.contributor.authorWassler, Michael
dc.contributor.authorGeng, Yong-Jian
dc.contributor.authorSulistyowati, Erna
dc.date.accessioned2021-10-14T01:45:01Z
dc.date.available2021-10-14T01:45:01Z
dc.date.issued2018-09-06
dc.identifier.urihttps://link.springer.com/article/10.1007/s12975-018-0660-9
dc.identifier.urihttp://repository.unisma.ac.id/handle/123456789/2033
dc.description[ARCHIVES] Copyright Article from: Translational Stroke Researchen_US
dc.description.abstractExtracellular 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.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofseriesTranslational Stroke Research;Vol.30, Pages 413-427
dc.subjectGene therapyen_US
dc.subjectReactive oxygen speciesen_US
dc.subjectRestenosisen_US
dc.subjectSuperoxide dismutaseen_US
dc.titleInhibition of Neointima Hyperplasia, Inflammation, and Reactive Oxygen Species in Balloon-Injured Arteries by HVJ Envelope Vector-Mediated Delivery of Superoxide Dismutase Geneen_US
dc.typeArticleen_US


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