Receptor-specific TRAIL as a means to achieve targeted elimination of activated hepatic stellate cells

Mohammad Arabpour; Robbert Cool; Klaas Nico Faber; Wim J Quax; Hidde J Haisma

doi:10.1080/1061186X.2016.1262867

Publication

Receptor-specific TRAIL as a means to achieve targeted elimination of activated hepatic stellate cells

Arabpour, M., Cool, R., Faber, K. N., Quax, W. J. & Haisma, H. J., 2017, In : Journal of Drug Targeting. 25, 4, p. 360-369 10 p.

Research output: Contribution to journal › Article › Academic › peer-review

APA

Arabpour, M., Cool, R., Faber, K. N., Quax, W. J., & Haisma, H. J. (2017). Receptor-specific TRAIL as a means to achieve targeted elimination of activated hepatic stellate cells. Journal of Drug Targeting, 25(4), 360-369. https://doi.org/10.1080/1061186X.2016.1262867

Author

Arabpour, Mohammad ; Cool, Robbert ; Faber, Klaas Nico ; Quax, Wim J ; Haisma, Hidde J. / Receptor-specific TRAIL as a means to achieve targeted elimination of activated hepatic stellate cells. In: Journal of Drug Targeting. 2017 ; Vol. 25, No. 4. pp. 360-369.

Harvard

Arabpour, M, Cool, R, Faber, KN, Quax, WJ & Haisma, HJ 2017, 'Receptor-specific TRAIL as a means to achieve targeted elimination of activated hepatic stellate cells', Journal of Drug Targeting, vol. 25, no. 4, pp. 360-369. https://doi.org/10.1080/1061186X.2016.1262867

Standard

Receptor-specific TRAIL as a means to achieve targeted elimination of activated hepatic stellate cells. / Arabpour, Mohammad; Cool, Robbert; Faber, Klaas Nico; Quax, Wim J; Haisma, Hidde J.

In: Journal of Drug Targeting, Vol. 25, No. 4, 2017, p. 360-369.

Research output: Contribution to journal › Article › Academic › peer-review

Vancouver

Arabpour M, Cool R, Faber KN, Quax WJ, Haisma HJ. Receptor-specific TRAIL as a means to achieve targeted elimination of activated hepatic stellate cells. Journal of Drug Targeting. 2017;25(4):360-369. https://doi.org/10.1080/1061186X.2016.1262867

BibTeX

@article{f664378146db41479722aa83190fbe12,

title = "Receptor-specific TRAIL as a means to achieve targeted elimination of activated hepatic stellate cells",

abstract = "Activated hepatic stellate cells (HSCs) are known to play a central role in liver fibrosis and their elimination is a crucial step toward the resolution and reversion of liver fibrosis. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a molecule that may contribute to the apoptotic removal of activated HSC through binding to its dedicated receptors. In the present study, we investigated the potential application of recombinant receptor-specific TRAIL proteins in the efficient elimination of activated HSCs. Our finding revealed differential contribution of TRAIL receptors among HSCs populations with activated hepatic stellate cells expresses more TRAIL receptors DR5. In vitro treatment of activated HSCs with DR5-specific or wild-type TRAIL variants induced a significant reduction in viability and extracellular matrix production, whereas no significant decrease in viability was associated with the treatment of cells by DR4-specific TRAIL. Our analysis indicate the successful application of the DR5 receptor-specific TRAIL variant in the targeted elimination of activated HSCs via interference with collagen production and simultaneous induction of apoptosis via activation of the caspase pathway. DR5 receptor-specific TRAIL may thus represent a new therapeutic compound for the treatment of liver fibrosis.",

keywords = "Liver fibrosis, hepatic stellate cell, receptor-specific TRAIL, targeted therapy, GROWTH-FACTOR-RECEPTOR, DEATH LIGAND TRAIL, MONOCLONAL-ANTIBODIES, COLLAGEN PRODUCTION, LIVER-REGENERATION, IN-VIVO, APOPTOSIS, RAT, PROLIFERATION, HEPATOCYTES",

author = "Mohammad Arabpour and Robbert Cool and Faber, {Klaas Nico} and Quax, {Wim J} and Haisma, {Hidde J}",

year = "2017",

doi = "10.1080/1061186X.2016.1262867",

language = "English",

volume = "25",

pages = "360--369",

journal = "Journal of Drug Targeting",

issn = "1061-186X",

publisher = "TAYLOR & FRANCIS LTD",

number = "4",

}

RIS

TY - JOUR

T1 - Receptor-specific TRAIL as a means to achieve targeted elimination of activated hepatic stellate cells

AU - Arabpour, Mohammad

AU - Cool, Robbert

AU - Faber, Klaas Nico

AU - Quax, Wim J

AU - Haisma, Hidde J

PY - 2017

Y1 - 2017

N2 - Activated hepatic stellate cells (HSCs) are known to play a central role in liver fibrosis and their elimination is a crucial step toward the resolution and reversion of liver fibrosis. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a molecule that may contribute to the apoptotic removal of activated HSC through binding to its dedicated receptors. In the present study, we investigated the potential application of recombinant receptor-specific TRAIL proteins in the efficient elimination of activated HSCs. Our finding revealed differential contribution of TRAIL receptors among HSCs populations with activated hepatic stellate cells expresses more TRAIL receptors DR5. In vitro treatment of activated HSCs with DR5-specific or wild-type TRAIL variants induced a significant reduction in viability and extracellular matrix production, whereas no significant decrease in viability was associated with the treatment of cells by DR4-specific TRAIL. Our analysis indicate the successful application of the DR5 receptor-specific TRAIL variant in the targeted elimination of activated HSCs via interference with collagen production and simultaneous induction of apoptosis via activation of the caspase pathway. DR5 receptor-specific TRAIL may thus represent a new therapeutic compound for the treatment of liver fibrosis.

AB - Activated hepatic stellate cells (HSCs) are known to play a central role in liver fibrosis and their elimination is a crucial step toward the resolution and reversion of liver fibrosis. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a molecule that may contribute to the apoptotic removal of activated HSC through binding to its dedicated receptors. In the present study, we investigated the potential application of recombinant receptor-specific TRAIL proteins in the efficient elimination of activated HSCs. Our finding revealed differential contribution of TRAIL receptors among HSCs populations with activated hepatic stellate cells expresses more TRAIL receptors DR5. In vitro treatment of activated HSCs with DR5-specific or wild-type TRAIL variants induced a significant reduction in viability and extracellular matrix production, whereas no significant decrease in viability was associated with the treatment of cells by DR4-specific TRAIL. Our analysis indicate the successful application of the DR5 receptor-specific TRAIL variant in the targeted elimination of activated HSCs via interference with collagen production and simultaneous induction of apoptosis via activation of the caspase pathway. DR5 receptor-specific TRAIL may thus represent a new therapeutic compound for the treatment of liver fibrosis.

KW - Liver fibrosis

KW - hepatic stellate cell

KW - receptor-specific TRAIL

KW - targeted therapy

KW - GROWTH-FACTOR-RECEPTOR

KW - DEATH LIGAND TRAIL

KW - MONOCLONAL-ANTIBODIES

KW - COLLAGEN PRODUCTION

KW - LIVER-REGENERATION

KW - IN-VIVO

KW - APOPTOSIS

KW - RAT

KW - PROLIFERATION

KW - HEPATOCYTES

U2 - 10.1080/1061186X.2016.1262867

DO - 10.1080/1061186X.2016.1262867

M3 - Article

VL - 25

SP - 360

EP - 369

JO - Journal of Drug Targeting

JF - Journal of Drug Targeting

SN - 1061-186X

IS - 4

ER -

ID: 37447912

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