Publication

Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis

de Vries, B., Walter, SJ., Wolfs, TGAM., Hochepied, T., Rabina, J., Heeringa, P., Parkkinen, J., Libert, C. & Buurman, WA., 27-Oct-2004, In : Transplantation. 78, 8, p. 1116-1124 9 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

de Vries, B., Walter, SJ., Wolfs, TGAM., Hochepied, T., Rabina, J., Heeringa, P., ... Buurman, WA. (2004). Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis. Transplantation, 78(8), 1116-1124. https://doi.org/10.1097/01.TP.0000138096.14126.CA

Author

de Vries, B ; Walter, SJ ; Wolfs, TGAM ; Hochepied, T ; Rabina, J ; Heeringa, P ; Parkkinen, J ; Libert, C ; Buurman, WA. / Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis. In: Transplantation. 2004 ; Vol. 78, No. 8. pp. 1116-1124.

Harvard

de Vries, B, Walter, SJ, Wolfs, TGAM, Hochepied, T, Rabina, J, Heeringa, P, Parkkinen, J, Libert, C & Buurman, WA 2004, 'Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis', Transplantation, vol. 78, no. 8, pp. 1116-1124. https://doi.org/10.1097/01.TP.0000138096.14126.CA

Standard

Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis. / de Vries, B; Walter, SJ; Wolfs, TGAM; Hochepied, T; Rabina, J; Heeringa, P; Parkkinen, J; Libert, C; Buurman, WA.

In: Transplantation, Vol. 78, No. 8, 27.10.2004, p. 1116-1124.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

de Vries B, Walter SJ, Wolfs TGAM, Hochepied T, Rabina J, Heeringa P et al. Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis. Transplantation. 2004 Oct 27;78(8):1116-1124. https://doi.org/10.1097/01.TP.0000138096.14126.CA


BibTeX

@article{e4924628b200484195093b27eb32750b,
title = "Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis",
abstract = "Background. Although ischemia-reperfusion (I/R) injury represents a major problem in posttransplant organ failure, effective treatment is not available. The acute phase protein a-l-acid glycoprotein (AGP) has been shown to be protective against experimental I/R injury. The effects of AGP are thought to be mediated by fucose groups expressed on the AGP protein inhibiting neutrophil infiltration. However, the precise mechanism of protection remains to be established. We therefore studied the effects of exogenous human AGP (hAGP) in a mouse model of ischemic acute renal failure.Methods. Mice were subjected to renal I/R and treated with hAGP, fucose-depleted hAGP, or control treated. Also, transgenic mice over-expressing rat AGP or wild-type controls were subjected to renal I/R.Results. Treatment was with hAGP as well as facose-depleted hAGP protected mice against I/R-induced acute renal failure. Surprisingly, AGP-over-expressing mice were not protected against I/R injury. Both natural and fucose-depleted hAGP inhibited the activation of the complement system, as determined by renal C3 deposition and influx of neutrophils measured by immunohistochemistry and myeloperoxidase-enzyme-linked immunoadsorbent assay. Tubular epithelial cell structure (actin cytoskeleton) and cell-cell interaction (tight-junction architecture) were completely preserved in AGP-treated mice. Also, epithelial caspase activation and apoptotic DNA cleavage were prevented by AGP treatment.Conclusions. Both natural and fucose-depleted hAGP protect against renal I/R injury by preservation of tubular epithelial structure and inhibition of apoptosis and subsequent inflammation. Therefore, hAGP can be regarded as a potential new therapeutic intervention in the treatment of acute renal failure, as seen after transplantation of ischemically injured kidneys.",
keywords = "ischemia-reperfusion, AGP, inflammation, neutrophil, apoptosis, ACUTE-PHASE PROTEINS, ALPHA(1)-ACID GLYCOPROTEIN, EPITHELIAL-CELLS, MYELOPEROXIDASE ACTIVITY, RAT-KIDNEY, CAMP, PERMEABILITY, ACTIVATION, MICE, ALPHA(1)-ANTITRYPSIN",
author = "{de Vries}, B and SJ Walter and TGAM Wolfs and T Hochepied and J Rabina and P Heeringa and J Parkkinen and C Libert and WA Buurman",
year = "2004",
month = "10",
day = "27",
doi = "10.1097/01.TP.0000138096.14126.CA",
language = "English",
volume = "78",
pages = "1116--1124",
journal = "Transplantation",
issn = "0041-1337",
publisher = "LIPPINCOTT WILLIAMS & WILKINS",
number = "8",

}

RIS

TY - JOUR

T1 - Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis

AU - de Vries, B

AU - Walter, SJ

AU - Wolfs, TGAM

AU - Hochepied, T

AU - Rabina, J

AU - Heeringa, P

AU - Parkkinen, J

AU - Libert, C

AU - Buurman, WA

PY - 2004/10/27

Y1 - 2004/10/27

N2 - Background. Although ischemia-reperfusion (I/R) injury represents a major problem in posttransplant organ failure, effective treatment is not available. The acute phase protein a-l-acid glycoprotein (AGP) has been shown to be protective against experimental I/R injury. The effects of AGP are thought to be mediated by fucose groups expressed on the AGP protein inhibiting neutrophil infiltration. However, the precise mechanism of protection remains to be established. We therefore studied the effects of exogenous human AGP (hAGP) in a mouse model of ischemic acute renal failure.Methods. Mice were subjected to renal I/R and treated with hAGP, fucose-depleted hAGP, or control treated. Also, transgenic mice over-expressing rat AGP or wild-type controls were subjected to renal I/R.Results. Treatment was with hAGP as well as facose-depleted hAGP protected mice against I/R-induced acute renal failure. Surprisingly, AGP-over-expressing mice were not protected against I/R injury. Both natural and fucose-depleted hAGP inhibited the activation of the complement system, as determined by renal C3 deposition and influx of neutrophils measured by immunohistochemistry and myeloperoxidase-enzyme-linked immunoadsorbent assay. Tubular epithelial cell structure (actin cytoskeleton) and cell-cell interaction (tight-junction architecture) were completely preserved in AGP-treated mice. Also, epithelial caspase activation and apoptotic DNA cleavage were prevented by AGP treatment.Conclusions. Both natural and fucose-depleted hAGP protect against renal I/R injury by preservation of tubular epithelial structure and inhibition of apoptosis and subsequent inflammation. Therefore, hAGP can be regarded as a potential new therapeutic intervention in the treatment of acute renal failure, as seen after transplantation of ischemically injured kidneys.

AB - Background. Although ischemia-reperfusion (I/R) injury represents a major problem in posttransplant organ failure, effective treatment is not available. The acute phase protein a-l-acid glycoprotein (AGP) has been shown to be protective against experimental I/R injury. The effects of AGP are thought to be mediated by fucose groups expressed on the AGP protein inhibiting neutrophil infiltration. However, the precise mechanism of protection remains to be established. We therefore studied the effects of exogenous human AGP (hAGP) in a mouse model of ischemic acute renal failure.Methods. Mice were subjected to renal I/R and treated with hAGP, fucose-depleted hAGP, or control treated. Also, transgenic mice over-expressing rat AGP or wild-type controls were subjected to renal I/R.Results. Treatment was with hAGP as well as facose-depleted hAGP protected mice against I/R-induced acute renal failure. Surprisingly, AGP-over-expressing mice were not protected against I/R injury. Both natural and fucose-depleted hAGP inhibited the activation of the complement system, as determined by renal C3 deposition and influx of neutrophils measured by immunohistochemistry and myeloperoxidase-enzyme-linked immunoadsorbent assay. Tubular epithelial cell structure (actin cytoskeleton) and cell-cell interaction (tight-junction architecture) were completely preserved in AGP-treated mice. Also, epithelial caspase activation and apoptotic DNA cleavage were prevented by AGP treatment.Conclusions. Both natural and fucose-depleted hAGP protect against renal I/R injury by preservation of tubular epithelial structure and inhibition of apoptosis and subsequent inflammation. Therefore, hAGP can be regarded as a potential new therapeutic intervention in the treatment of acute renal failure, as seen after transplantation of ischemically injured kidneys.

KW - ischemia-reperfusion

KW - AGP

KW - inflammation

KW - neutrophil

KW - apoptosis

KW - ACUTE-PHASE PROTEINS

KW - ALPHA(1)-ACID GLYCOPROTEIN

KW - EPITHELIAL-CELLS

KW - MYELOPEROXIDASE ACTIVITY

KW - RAT-KIDNEY

KW - CAMP

KW - PERMEABILITY

KW - ACTIVATION

KW - MICE

KW - ALPHA(1)-ANTITRYPSIN

U2 - 10.1097/01.TP.0000138096.14126.CA

DO - 10.1097/01.TP.0000138096.14126.CA

M3 - Article

VL - 78

SP - 1116

EP - 1124

JO - Transplantation

JF - Transplantation

SN - 0041-1337

IS - 8

ER -

ID: 13909066