Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0028560
Title: Gene transfer using micellar nanovectors inhibits choroidal neovascularization in vivo
Authors: Iriyama A.
Oba M.
Ishii T.
Nishiyama N.
Kataoka K.
Tamaki Y.
Yanagi Y. 
Keywords: alanine aminotransferase
aspartate aminotransferase
creatinine
urea
vasculotropin receptor 1
yellow fluorescent protein
bacterial protein
DNA
fluorescein
photoprotein
polymer
yellow fluorescent protein, Bacteria
animal experiment
animal model
article
controlled study
fluorescence microscopy
gene expression
gene transfer
histopathology
immunohistochemistry
in vivo study
laser coagulation
male
micelle
mouse
nonhuman
pigment epithelium
plasmid
protein expression
quantitative analysis
retina fluorescein angiography
retina macula age related degeneration
signal transduction
subretinal neovascularization
urea nitrogen blood level
Western blotting
animal
C57BL mouse
chemistry
disease course
disease model
gene transfer
gene vector
metabolism
methodology
pathology
retina macula degeneration
Animals
Bacterial Proteins
Choroidal Neovascularization
Disease Models, Animal
Disease Progression
DNA
Fluorescein
Gene Transfer Techniques
Genetic Vectors
Laser Coagulation
Light Coagulation
Luminescent Proteins
Macular Degeneration
Male
Mice
Mice, Inbred C57BL
Micelles
Microscopy, Fluorescence
Polymers
Issue Date: 2011
Citation: Iriyama A., Oba M., Ishii T., Nishiyama N., Kataoka K., Tamaki Y., Yanagi Y. (2011). Gene transfer using micellar nanovectors inhibits choroidal neovascularization in vivo. PLoS ONE 6 (12) : e28560. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0028560
Rights: Attribution 4.0 International
Abstract: Purpose: Age-related macular degeneration caused by choroidal neovascularization (CNV) remains difficult to be treated despite the recent advent of several treatment options. In this study, we investigated the in vivo angiogenic control by intravenous injection of polyion complex (PIC) micelle encapsulating plasmid DNA (pDNA) using a mice CNV model. Methods: The transfection efficiency of the PIC micelle was investigated using the laser-induced CNV in eight-week-old male C57 BJ/6 mice. Firstly, each mouse received intravenous injection of micelle encapsulating pDNA of Yellow Fluorescent Protein (pYFP) on days 1,3 and 5. The expression of YFP was analyzed using fluorescein microscopy and western blotting analysis. In the next experiments, each mouse received intravenous injection of micelle encapsulating pDNA of soluble Fms-like tyrosine kinase-1 (psFlt-1) 1,3 and 5 days after the induction of CNV and the CNV lesion was analyzed by choroidal flatmounts on day 7. Results: Fluorescein microscopy and western blotting analysis revealed that the expression of YFP was confirmed in the CNV area after injection of the PIC micelle, but the expression was not detected neither in mice that received naked pDNA nor those without CNV. Furthermore, the CNV area in the mice that received intravenous injection of the psFlt-1-encapsulated PIC micelle was significantly reduced by 65% compared to that in control mice (p<0.01). Conclusions: Transfection of sFlt-1 with the PIC micelle by intravenous injection to mice CNV models showed significant inhibition of CNV. The current results revealed the significant potential of nonviral gene therapy for regulation of CNV using the PIC micelle encapsulating pDNA. © 2011 Iriyama et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Source Title: PLoS ONE
URI: https://scholarbank.nus.edu.sg/handle/10635/162022
ISSN: 19326203
DOI: 10.1371/journal.pone.0028560
Rights: Attribution 4.0 International
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This item is licensed under a Creative Commons License Creative Commons