Skeletal muscle regeneration after insulin-like growth factor I gene transfer by recombinant Sendai virus vector

Shiotani, Akiko; Fukumura, Masayuki; Maeda, Masayuki; Hou, Xiaogang; Inoue, Makoto; Kanamori, Tatsuyuki; Komaba, Sumika; Washizawa, K; Fujikawa, Satoshi; Yamamoto, Takuya; Kadono, Chiho; Watabe, Kazuhiko; Fukuda, Hiroyuki; Saito, Koichiro; Sakai, Yuko; Nagai, Yoshinori; Kanzaki, Jin; Hasegawa, Mamoru

doi:10.1038/sj.gt.3301486

Cited by 53 publications

(48 citation statements)

References 29 publications

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“…4,5 Sendai virus (SeV), also a member of the Paramyxoviridae, infects most mammalian cells and directs highlevel expression not only in cultured cells but also in experimental animals of the genes within its genome that have been exploited for therapeutic use and vaccination. [6][7][8][9][10] A strong potential of NDV as a vaccine vector was also demonstrated. 11 SeV and most of the other mononegaviruses replicate independent of cellular nuclear functions and do not have a DNA phase in their lifecycle, and therefore are not considered to present a high risk of cell transformation by integration of the viral genetic information into the cellular genome.…”

Section: Introductionmentioning

confidence: 95%

Generation of a recombinant Sendai virus that is selectively activated and lyses human tumor cells expressing matrix metalloproteinases

et al. 2004

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Malignant tumor cells often express matrix metalloproteinases (MMPs) at a high level to enable their dissemination and metastasis. Sendai virus (SeV), a nonsegmented negative strand RNA virus, spreads in the target tissues in vivo via cleavage activation of the viral fusion glycoprotein by a tissue-specific, trypsin-like enzyme. By deleting the viral matrix protein, we previously generated a recombinant SeV that does not bud to mature virions, but is highly fusogenic and spreads extensively from cell to cell in a trypsindependent manner. Here, we changed the tryptic cleavage site of the fusion glycoprotein of this virus to a site susceptible to MMPs. The resulting recombinant virus was no longer activated by trypsin but spread efficiently in cultured cells supplemented with MMP2 or MMP9 and in human tumor cell lines expressing these MMPs. Furthermore, the virus spread extensively in tumor cells xenotrasplanted to nude mice without disseminating to the surrounding normal cells, leading to the inhibition of the tumor growth in the mice. These results demonstrate the selective targeting and killing of human tumor cells by recombinant SeV technology and greatly advance the reemerging concept of oncolytic virotherapy, which currently appears to rely largely upon a natural preference of certain viruses for cancer cells.

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Section: Introductionmentioning

confidence: 95%

Generation of a recombinant Sendai virus that is selectively activated and lyses human tumor cells expressing matrix metalloproteinases

et al. 2004

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“…(i) SeV vectors can infect nondividing, quiescent cells as well as dividing cells unlike oncoretroviral vectors. [7][8][9][10][11] Thus, they can be used to infect cells that are terminally differentiated as well as at various stages of differentiation, whether they are dividing or not.…”

Section: Discussionmentioning

confidence: 99%

“…[3][4][5] We have previously developed Sendai virus (SeV) vectors that replicate in the form of negative-sense single-stranded RNA in the cytoplasm of infected cells and do not go through a DNA phase. 6 SeV vectors can efficiently introduce foreign genes without toxicity into airway epithelial cells, 7 vascular tissue, 8 skeletal muscle, 9 synovial cells, 10 retinal tissue, 11 and hematopoietic progenitor cells. 12 Here we report that the SeV-mediated gene transfer into primate ES cells is very efficient and stable even after the terminal differentiation of the cells.…”

Section: Introductionmentioning

confidence: 99%

Efficient and stable Sendai virus-mediated gene transfer into primate embryonic stem cells with pluripotency preserved

et al. 2004

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Efficient gene transfer and regulated transgene expression in primate embryonic stem (ES) cells are highly desirable for future applications of the cells. In the present study, we have examined using the nonintegrating Sendai virus (SeV) vector to introduce the green fluorescent protein (GFP) gene into non-human primate cynomolgus ES cells. The GFP gene was vigorously and stably expressed in the cynomolgus ES cells for a year. The cells were able to form fluorescent teratomas when transplanted into immunodeficient mice. They were also able to differentiate into fluorescent embryoid bodies, neurons, and mature blood cells. In addition, the GFP expression levels were reduced dose-dependently by the addition of an anti-RNA virus drug, ribavirin, to the culture. Thus, SeV vector will be a useful tool for efficient gene transfer into primate ES cells and the method of using antiviral drugs should allow further investigation for regulated SeV-mediated gene expression.

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“…In addition, there may be innate immunity, humoral or cellular immunity to viral proteins and transgenes. First-generation SeVV has been shown to stimulate a potent inflammatory immune response including tissue necrosis 18 and infiltration of lymphocytes, macrophages and neutrophils. 6,19 Advancing therapeutic application of virus to the fetal period has been shown to overcome immunological obstacles by pre-empting the development of a mature immune system.…”

Section: Prenatal Delivery Of Sendai Virus Vectors Sn Waddington Et Almentioning

confidence: 99%

Reduced toxicity of F-deficient Sendai virus vector in the mouse fetus

et al. 2004

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Skeletal muscle regeneration after insulin-like growth factor I gene transfer by recombinant Sendai virus vector

Cited by 53 publications

References 29 publications

Generation of a recombinant Sendai virus that is selectively activated and lyses human tumor cells expressing matrix metalloproteinases

Generation of a recombinant Sendai virus that is selectively activated and lyses human tumor cells expressing matrix metalloproteinases

Efficient and stable Sendai virus-mediated gene transfer into primate embryonic stem cells with pluripotency preserved

Reduced toxicity of F-deficient Sendai virus vector in the mouse fetus

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