Publication

Targeted adenovirus mediated inhibition of NF-kappa B-dependent inflammatory gene expression in endothelial cells in vitro and in vivo

Kuldo, J. M., Asgeirsdottir, S. A., Zwiers, P. J., Bellu, A. R., Rots, M. G., Schalk, J. A. C., Ogawara, K. I., Trautwein, C., Banas, B., Haisma, H. J., Molema, G. & Kamps, J. A. A. M., 28-Feb-2013, In : Journal of Controlled Release. 166, 1, p. 57-65 9 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Kuldo, J. M., Asgeirsdottir, S. A., Zwiers, P. J., Bellu, A. R., Rots, M. G., Schalk, J. A. C., ... Kamps, J. A. A. M. (2013). Targeted adenovirus mediated inhibition of NF-kappa B-dependent inflammatory gene expression in endothelial cells in vitro and in vivo. Journal of Controlled Release, 166(1), 57-65. https://doi.org/10.1016/j.jconrel.2012.12.016

Author

Kuldo, J. M. ; Asgeirsdottir, S. A. ; Zwiers, P. J. ; Bellu, A. R. ; Rots, M. G. ; Schalk, J. A. C. ; Ogawara, K. I. ; Trautwein, C. ; Banas, B. ; Haisma, H. J. ; Molema, G. ; Kamps, J. A. A. M. / Targeted adenovirus mediated inhibition of NF-kappa B-dependent inflammatory gene expression in endothelial cells in vitro and in vivo. In: Journal of Controlled Release. 2013 ; Vol. 166, No. 1. pp. 57-65.

Harvard

Kuldo, JM, Asgeirsdottir, SA, Zwiers, PJ, Bellu, AR, Rots, MG, Schalk, JAC, Ogawara, KI, Trautwein, C, Banas, B, Haisma, HJ, Molema, G & Kamps, JAAM 2013, 'Targeted adenovirus mediated inhibition of NF-kappa B-dependent inflammatory gene expression in endothelial cells in vitro and in vivo', Journal of Controlled Release, vol. 166, no. 1, pp. 57-65. https://doi.org/10.1016/j.jconrel.2012.12.016

Standard

Targeted adenovirus mediated inhibition of NF-kappa B-dependent inflammatory gene expression in endothelial cells in vitro and in vivo. / Kuldo, J. M.; Asgeirsdottir, S. A.; Zwiers, P. J.; Bellu, A. R.; Rots, M. G.; Schalk, J. A. C.; Ogawara, K. I.; Trautwein, C.; Banas, B.; Haisma, H. J.; Molema, G.; Kamps, J. A. A. M.

In: Journal of Controlled Release, Vol. 166, No. 1, 28.02.2013, p. 57-65.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Kuldo JM, Asgeirsdottir SA, Zwiers PJ, Bellu AR, Rots MG, Schalk JAC et al. Targeted adenovirus mediated inhibition of NF-kappa B-dependent inflammatory gene expression in endothelial cells in vitro and in vivo. Journal of Controlled Release. 2013 Feb 28;166(1):57-65. https://doi.org/10.1016/j.jconrel.2012.12.016


BibTeX

@article{f716c0509ea848e48688a1c8eed932aa,
title = "Targeted adenovirus mediated inhibition of NF-kappa B-dependent inflammatory gene expression in endothelial cells in vitro and in vivo",
abstract = "In chronic inflammatory diseases the endothelium expresses mediators responsible for harmful leukocyte infiltration. We investigated whether targeted delivery of a therapeutic transgene that inhibits nuclear factor kappa B signal transduction could silence the proinflammatory activation status of endothelial cells. For this, an adenovirus encoding dominant-negative I kappa B (dnI kappa B) as a therapeutic transgene was employed. Selectivity for the endothelial cells was achieved by introduction of antibodies specific for inflammatory endothelial adhesion molecules E-selectin or VCAM-1 chemically linked to the virus via polyethylene glycol. In vitro, the retargeted adenoviruses selectively infected cytokine-activated endothelial cells to express functional transgene. The comparison of transductional capacity of both retargeted viruses revealed that E-selectin based transgene delivery exerted superior pharmacological effects. Targeted delivery mediated dnI kappa B transgene expression in endothelial cells inhibited the induced expression of several inflammatory genes, including adhesion molecules, cytokines, and chemokines. In vivo, in mice suffering from glomerulonephritis, E-selectin-retargeted adenovirus selectively homed in the kidney to microvascular glomerular endothelium. Subsequent downregulation of endothelial adhesion molecule expression 2 days after induction of inflammation demonstrated the pharmacological potential of this gene therapy approach. The data justify further studies towards therapeutic virus design and optimization of treatment schedules to investigate their capacity to interfere with inflammatory disease progression. (C) 2012 Elsevier B.V. All rights reserved.",
keywords = "Inflammation, Endothelium, NF-kappa B inhibition, Adenoviral gene therapy, E-selectin targeting, ANTI-GBM GLOMERULONEPHRITIS, LUPUS NEPHRITIS, DRUG-DELIVERY, DEXAMETHASONE, ACTIVATION, IMMUNOLIPOSOMES, NEPHROPATHY, APOPTOSIS, VECTORS, P38",
author = "Kuldo, {J. M.} and Asgeirsdottir, {S. A.} and Zwiers, {P. J.} and Bellu, {A. R.} and Rots, {M. G.} and Schalk, {J. A. C.} and Ogawara, {K. I.} and C. Trautwein and B. Banas and Haisma, {H. J.} and G. Molema and Kamps, {J. A. A. M.}",
year = "2013",
month = "2",
day = "28",
doi = "10.1016/j.jconrel.2012.12.016",
language = "English",
volume = "166",
pages = "57--65",
journal = "Journal of Controlled Release",
issn = "0168-3659",
publisher = "Elsevier Bedrijfsinformatie b.v.",
number = "1",

}

RIS

TY - JOUR

T1 - Targeted adenovirus mediated inhibition of NF-kappa B-dependent inflammatory gene expression in endothelial cells in vitro and in vivo

AU - Kuldo, J. M.

AU - Asgeirsdottir, S. A.

AU - Zwiers, P. J.

AU - Bellu, A. R.

AU - Rots, M. G.

AU - Schalk, J. A. C.

AU - Ogawara, K. I.

AU - Trautwein, C.

AU - Banas, B.

AU - Haisma, H. J.

AU - Molema, G.

AU - Kamps, J. A. A. M.

PY - 2013/2/28

Y1 - 2013/2/28

N2 - In chronic inflammatory diseases the endothelium expresses mediators responsible for harmful leukocyte infiltration. We investigated whether targeted delivery of a therapeutic transgene that inhibits nuclear factor kappa B signal transduction could silence the proinflammatory activation status of endothelial cells. For this, an adenovirus encoding dominant-negative I kappa B (dnI kappa B) as a therapeutic transgene was employed. Selectivity for the endothelial cells was achieved by introduction of antibodies specific for inflammatory endothelial adhesion molecules E-selectin or VCAM-1 chemically linked to the virus via polyethylene glycol. In vitro, the retargeted adenoviruses selectively infected cytokine-activated endothelial cells to express functional transgene. The comparison of transductional capacity of both retargeted viruses revealed that E-selectin based transgene delivery exerted superior pharmacological effects. Targeted delivery mediated dnI kappa B transgene expression in endothelial cells inhibited the induced expression of several inflammatory genes, including adhesion molecules, cytokines, and chemokines. In vivo, in mice suffering from glomerulonephritis, E-selectin-retargeted adenovirus selectively homed in the kidney to microvascular glomerular endothelium. Subsequent downregulation of endothelial adhesion molecule expression 2 days after induction of inflammation demonstrated the pharmacological potential of this gene therapy approach. The data justify further studies towards therapeutic virus design and optimization of treatment schedules to investigate their capacity to interfere with inflammatory disease progression. (C) 2012 Elsevier B.V. All rights reserved.

AB - In chronic inflammatory diseases the endothelium expresses mediators responsible for harmful leukocyte infiltration. We investigated whether targeted delivery of a therapeutic transgene that inhibits nuclear factor kappa B signal transduction could silence the proinflammatory activation status of endothelial cells. For this, an adenovirus encoding dominant-negative I kappa B (dnI kappa B) as a therapeutic transgene was employed. Selectivity for the endothelial cells was achieved by introduction of antibodies specific for inflammatory endothelial adhesion molecules E-selectin or VCAM-1 chemically linked to the virus via polyethylene glycol. In vitro, the retargeted adenoviruses selectively infected cytokine-activated endothelial cells to express functional transgene. The comparison of transductional capacity of both retargeted viruses revealed that E-selectin based transgene delivery exerted superior pharmacological effects. Targeted delivery mediated dnI kappa B transgene expression in endothelial cells inhibited the induced expression of several inflammatory genes, including adhesion molecules, cytokines, and chemokines. In vivo, in mice suffering from glomerulonephritis, E-selectin-retargeted adenovirus selectively homed in the kidney to microvascular glomerular endothelium. Subsequent downregulation of endothelial adhesion molecule expression 2 days after induction of inflammation demonstrated the pharmacological potential of this gene therapy approach. The data justify further studies towards therapeutic virus design and optimization of treatment schedules to investigate their capacity to interfere with inflammatory disease progression. (C) 2012 Elsevier B.V. All rights reserved.

KW - Inflammation

KW - Endothelium

KW - NF-kappa B inhibition

KW - Adenoviral gene therapy

KW - E-selectin targeting

KW - ANTI-GBM GLOMERULONEPHRITIS

KW - LUPUS NEPHRITIS

KW - DRUG-DELIVERY

KW - DEXAMETHASONE

KW - ACTIVATION

KW - IMMUNOLIPOSOMES

KW - NEPHROPATHY

KW - APOPTOSIS

KW - VECTORS

KW - P38

U2 - 10.1016/j.jconrel.2012.12.016

DO - 10.1016/j.jconrel.2012.12.016

M3 - Article

VL - 166

SP - 57

EP - 65

JO - Journal of Controlled Release

JF - Journal of Controlled Release

SN - 0168-3659

IS - 1

ER -

ID: 5802135