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• W2965159306 abstract "Intimal hyperplasia is a complex process which contributes to several clinical problems such as atherosclerosis and postangioplasty restenosis. Inhibition of Smad3 expression inhibits intimal thickening. Our previous study has modified biscarbamate cross-linked polyethylenimine derivative (PEI-Et) through PEGylation thus obtained polyethylene glycol-graft-polyethylenimine derivative (PEG-Et 1:1), which has lower cytotoxicity and higher gene transfection efficiency compared with PEI-Et. In this study, PEG-Et 1:1 was employed in Smad3 shRNA (shSmad3) delivery for preventing intimal hyperplasia after vascular injury. It was observed that PEG-Et 1:1 could condense shSmad3 gene into nanoparticles with particle size of 115-168 nm and zeta potential of 3-6 mV. PEG-Et 1:1 displayed remarkably lower cytotoxicity, higher transfection efficiency, and shRNA silencing efficiency than PEI-Et and PEI 25 kDa in vascular smooth muscle cells (VSMCs). Moreover, PEG-Et 1:1/shSmad3 polyplex treatment significantly inhibited collagen, matrix metalloproteinase 1 (MMP1), MMP2 and MMP9 expression, and upregulated tissue inhibitor of metalloproteinase 1 (TIMP1) expression both in vitro and in vivo. Furthermore, intravascular delivery of shSmad3 with PEG-Et 1:1 polyplex efficiently reduced Smad3 expression and inhibited intimal thickening 14 days after vascular injury. Ultimately, this study indicated that PEG-Et 1:1-mediated local delivery of shSmad3 is a promising strategy for preventing intimal thickening." @default.
• W2965159306 created "2019-08-13" @default.
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• W2965159306 date "2019-07-29" @default.
• W2965159306 modified "2023-09-23" @default.
• W2965159306 title "PEGylated Polyethylenimine Derivative-Mediated Local Delivery of the shSmad3 Inhibits Intimal Thickening after Vascular Injury" @default.
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• W2965159306 doi "https://doi.org/10.1155/2019/8483765" @default.
• W2965159306 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6699321" @default.
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