Jørgen Frøkiær

Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy

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Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy. / Nilsson, Line; Madsen, Kirsten; Krag, Søren Rasmus Palmelund; Frøkiær, Jørgen; Jensen, Boye L; Nørregaard, Rikke; Munk, Ole Lajord.

In: American Journal of Physiology: Renal Physiology, Vol. 309, No. 12, 15.12.2015, p. F1035-48.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Nilsson, L, Madsen, K, Krag, SRP, Frøkiær, J, Jensen, BL, Nørregaard, R & Munk, OL 2015, 'Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy', American Journal of Physiology: Renal Physiology, vol. 309, no. 12, pp. F1035-48. https://doi.org/10.1152/ajprenal.00253.2015

APA

Nilsson, L., Madsen, K., Krag, S. R. P., Frøkiær, J., Jensen, B. L., Nørregaard, R., & Munk, O. L. (2015). Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy. American Journal of Physiology: Renal Physiology, 309(12), F1035-48. https://doi.org/10.1152/ajprenal.00253.2015

CBE

MLA

Vancouver

Nilsson L, Madsen K, Krag SRP, Frøkiær J, Jensen BL, Nørregaard R et al. Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy. American Journal of Physiology: Renal Physiology. 2015 Dec 15;309(12):F1035-48. https://doi.org/10.1152/ajprenal.00253.2015

Author

Nilsson, Line ; Madsen, Kirsten ; Krag, Søren Rasmus Palmelund ; Frøkiær, Jørgen ; Jensen, Boye L ; Nørregaard, Rikke ; Munk, Ole Lajord. / Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy. In: American Journal of Physiology: Renal Physiology. 2015 ; Vol. 309, No. 12. pp. F1035-48.

Bibtex

@article{9c048092a5f64c7ab42b33eaca8bc77f,
title = "Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy",
abstract = "Renal oxidative stress is increased in response to ureteral obstruction. In vitro, cyclooxygenase (COX)-2 activity contributes to protection against oxidants. In the present study, we tested the hypothesis that COX-2 activity counters oxidative stress and apoptosis in an in vivo model of obstructive nephropathy. Renal oxidative stress markers, antioxidant enzymes, and markers of tubular injury, tubular dilation, and apoptosis were investigated in COX-2 knockout (COX-2(-/-)) and wild-type (WT) mice subjected to 3 or 7 days of unilateral ureteral obstruction (UUO). In a separate series, WT sham-operated and UUO mice were treated with a selective COX-2 inhibitor, parecoxib. COX-2 increased in response to UUO; the oxidative stress markers 4-hydroxynonenal and nitrotyrosine protein residues increased in kidney tissue with no genotype difference after UUO, whereas the antioxidant enzymes heme oxygenase-1 and SOD2 displayed higher levels in COX-2(-/-) mice. Tubular injury was aggravated by COX-2 deletion, as measured by tubular dilatation, an increase in kidney injury molecule-1, cortical caspase-3 content, and apoptosis index. In conclusion, COX-2 is necessary to protect against tubular injury and apoptosis after UUO but not necessary to protect against oxidative stress. COX-2 is not likely to directly regulate antioxidant enzymes heme oxygenase-1 and SOD in the kidney.",
author = "Line Nilsson and Kirsten Madsen and Krag, {S{\o}ren Rasmus Palmelund} and J{\o}rgen Fr{\o}ki{\ae}r and Jensen, {Boye L} and Rikke N{\o}rregaard and Munk, {Ole Lajord}",
note = "Copyright {\textcopyright} 2015 the American Physiological Society.",
year = "2015",
month = dec,
day = "15",
doi = "10.1152/ajprenal.00253.2015",
language = "English",
volume = "309",
pages = "F1035--48",
journal = "American Journal of Physiology: Renal Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "12",

}

RIS

TY - JOUR

T1 - Disruption of cyclooxygenase type 2 exacerbates apoptosis and renal damage during obstructive nephropathy

AU - Nilsson, Line

AU - Madsen, Kirsten

AU - Krag, Søren Rasmus Palmelund

AU - Frøkiær, Jørgen

AU - Jensen, Boye L

AU - Nørregaard, Rikke

AU - Munk, Ole Lajord

N1 - Copyright © 2015 the American Physiological Society.

PY - 2015/12/15

Y1 - 2015/12/15

N2 - Renal oxidative stress is increased in response to ureteral obstruction. In vitro, cyclooxygenase (COX)-2 activity contributes to protection against oxidants. In the present study, we tested the hypothesis that COX-2 activity counters oxidative stress and apoptosis in an in vivo model of obstructive nephropathy. Renal oxidative stress markers, antioxidant enzymes, and markers of tubular injury, tubular dilation, and apoptosis were investigated in COX-2 knockout (COX-2(-/-)) and wild-type (WT) mice subjected to 3 or 7 days of unilateral ureteral obstruction (UUO). In a separate series, WT sham-operated and UUO mice were treated with a selective COX-2 inhibitor, parecoxib. COX-2 increased in response to UUO; the oxidative stress markers 4-hydroxynonenal and nitrotyrosine protein residues increased in kidney tissue with no genotype difference after UUO, whereas the antioxidant enzymes heme oxygenase-1 and SOD2 displayed higher levels in COX-2(-/-) mice. Tubular injury was aggravated by COX-2 deletion, as measured by tubular dilatation, an increase in kidney injury molecule-1, cortical caspase-3 content, and apoptosis index. In conclusion, COX-2 is necessary to protect against tubular injury and apoptosis after UUO but not necessary to protect against oxidative stress. COX-2 is not likely to directly regulate antioxidant enzymes heme oxygenase-1 and SOD in the kidney.

AB - Renal oxidative stress is increased in response to ureteral obstruction. In vitro, cyclooxygenase (COX)-2 activity contributes to protection against oxidants. In the present study, we tested the hypothesis that COX-2 activity counters oxidative stress and apoptosis in an in vivo model of obstructive nephropathy. Renal oxidative stress markers, antioxidant enzymes, and markers of tubular injury, tubular dilation, and apoptosis were investigated in COX-2 knockout (COX-2(-/-)) and wild-type (WT) mice subjected to 3 or 7 days of unilateral ureteral obstruction (UUO). In a separate series, WT sham-operated and UUO mice were treated with a selective COX-2 inhibitor, parecoxib. COX-2 increased in response to UUO; the oxidative stress markers 4-hydroxynonenal and nitrotyrosine protein residues increased in kidney tissue with no genotype difference after UUO, whereas the antioxidant enzymes heme oxygenase-1 and SOD2 displayed higher levels in COX-2(-/-) mice. Tubular injury was aggravated by COX-2 deletion, as measured by tubular dilatation, an increase in kidney injury molecule-1, cortical caspase-3 content, and apoptosis index. In conclusion, COX-2 is necessary to protect against tubular injury and apoptosis after UUO but not necessary to protect against oxidative stress. COX-2 is not likely to directly regulate antioxidant enzymes heme oxygenase-1 and SOD in the kidney.

U2 - 10.1152/ajprenal.00253.2015

DO - 10.1152/ajprenal.00253.2015

M3 - Journal article

C2 - 26671967

VL - 309

SP - F1035-48

JO - American Journal of Physiology: Renal Physiology

JF - American Journal of Physiology: Renal Physiology

SN - 1931-857X

IS - 12

ER -