Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema

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Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema. / Eefsen, Martin; Jelnes, Peter; Schmidt, Lars E; Vainer, Ben; Bisgaard, Hanne Cathrine; Larsen, Fin S.

In: Metabolic Brain Disease, Vol. 25, No. 3, 01.09.2010, p. 315-23.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Eefsen, M, Jelnes, P, Schmidt, LE, Vainer, B, Bisgaard, HC & Larsen, FS 2010, 'Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema', Metabolic Brain Disease, vol. 25, no. 3, pp. 315-23. https://doi.org/10.1007/s11011-010-9213-y, https://doi.org/10.1007/s11011-010-9213-y

APA

Eefsen, M., Jelnes, P., Schmidt, L. E., Vainer, B., Bisgaard, H. C., & Larsen, F. S. (2010). Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema. Metabolic Brain Disease, 25(3), 315-23. https://doi.org/10.1007/s11011-010-9213-y, https://doi.org/10.1007/s11011-010-9213-y

Vancouver

Eefsen M, Jelnes P, Schmidt LE, Vainer B, Bisgaard HC, Larsen FS. Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema. Metabolic Brain Disease. 2010 Sep 1;25(3):315-23. https://doi.org/10.1007/s11011-010-9213-y, https://doi.org/10.1007/s11011-010-9213-y

Author

Eefsen, Martin ; Jelnes, Peter ; Schmidt, Lars E ; Vainer, Ben ; Bisgaard, Hanne Cathrine ; Larsen, Fin S. / Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema. In: Metabolic Brain Disease. 2010 ; Vol. 25, No. 3. pp. 315-23.

Bibtex

@article{3d215487e79946eeaa597123b9565d22,
title = "Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema",
abstract = "Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and/or Aqp4 in ALF mediated brain edema. We induced acute liver injury and hyperammonemia in mice, to evaluate brain edema formation and the parallel expression of Aqp1 and Aqp4 in ALF. Liver injury and hyperammonemia were induced by +D-galactosamine (GLN) plus lipopolysaccharide (LPS) intraperitoneally and intravenous ammonia-acetate (NH(4)(+)), the GLN+LPS+NH(4)(+) group. The vehicle control group (CONTROL) was treated with NaCl and phosphate-buffered saline. The GLN+LPS+NH(4)(+) group showed significantly elevated p-alanine aminotransferase, p-INR and p-ammonium vs. CONTROL (p <0.001). Cortical brain water content was significantly elevated in the GLN+LPS+NH(4)(+) group vs. CONTROL, mean (SEM) 80.8(0.3) vs 80.0(0.1) % (p <0.05). Western blot of membrane enriched cortical brain tissue showed significantly upregulation of Aqp4 in the GLN+LPS+NH(4)(+) group vs. CONTROL, mean AU (SEM) 100775(14820) vs. 58857(6266) (p <0.05), and stationary levels for Aqp1. Aqp1 and Aqp4 mRNA were stationary. This study indicates that Aqp4, but not Aqp1, may be of importance in the pathogenesis of cortical brain edema in mice with ALF.",
author = "Martin Eefsen and Peter Jelnes and Schmidt, {Lars E} and Ben Vainer and Bisgaard, {Hanne Cathrine} and Larsen, {Fin S}",
year = "2010",
month = sep,
day = "1",
doi = "10.1007/s11011-010-9213-y",
language = "English",
volume = "25",
pages = "315--23",
journal = "Metabolic Brain Disease",
issn = "0885-7490",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema

AU - Eefsen, Martin

AU - Jelnes, Peter

AU - Schmidt, Lars E

AU - Vainer, Ben

AU - Bisgaard, Hanne Cathrine

AU - Larsen, Fin S

PY - 2010/9/1

Y1 - 2010/9/1

N2 - Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and/or Aqp4 in ALF mediated brain edema. We induced acute liver injury and hyperammonemia in mice, to evaluate brain edema formation and the parallel expression of Aqp1 and Aqp4 in ALF. Liver injury and hyperammonemia were induced by +D-galactosamine (GLN) plus lipopolysaccharide (LPS) intraperitoneally and intravenous ammonia-acetate (NH(4)(+)), the GLN+LPS+NH(4)(+) group. The vehicle control group (CONTROL) was treated with NaCl and phosphate-buffered saline. The GLN+LPS+NH(4)(+) group showed significantly elevated p-alanine aminotransferase, p-INR and p-ammonium vs. CONTROL (p <0.001). Cortical brain water content was significantly elevated in the GLN+LPS+NH(4)(+) group vs. CONTROL, mean (SEM) 80.8(0.3) vs 80.0(0.1) % (p <0.05). Western blot of membrane enriched cortical brain tissue showed significantly upregulation of Aqp4 in the GLN+LPS+NH(4)(+) group vs. CONTROL, mean AU (SEM) 100775(14820) vs. 58857(6266) (p <0.05), and stationary levels for Aqp1. Aqp1 and Aqp4 mRNA were stationary. This study indicates that Aqp4, but not Aqp1, may be of importance in the pathogenesis of cortical brain edema in mice with ALF.

AB - Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and/or Aqp4 in ALF mediated brain edema. We induced acute liver injury and hyperammonemia in mice, to evaluate brain edema formation and the parallel expression of Aqp1 and Aqp4 in ALF. Liver injury and hyperammonemia were induced by +D-galactosamine (GLN) plus lipopolysaccharide (LPS) intraperitoneally and intravenous ammonia-acetate (NH(4)(+)), the GLN+LPS+NH(4)(+) group. The vehicle control group (CONTROL) was treated with NaCl and phosphate-buffered saline. The GLN+LPS+NH(4)(+) group showed significantly elevated p-alanine aminotransferase, p-INR and p-ammonium vs. CONTROL (p <0.001). Cortical brain water content was significantly elevated in the GLN+LPS+NH(4)(+) group vs. CONTROL, mean (SEM) 80.8(0.3) vs 80.0(0.1) % (p <0.05). Western blot of membrane enriched cortical brain tissue showed significantly upregulation of Aqp4 in the GLN+LPS+NH(4)(+) group vs. CONTROL, mean AU (SEM) 100775(14820) vs. 58857(6266) (p <0.05), and stationary levels for Aqp1. Aqp1 and Aqp4 mRNA were stationary. This study indicates that Aqp4, but not Aqp1, may be of importance in the pathogenesis of cortical brain edema in mice with ALF.

U2 - 10.1007/s11011-010-9213-y

DO - 10.1007/s11011-010-9213-y

M3 - Journal article

C2 - 20938728

VL - 25

SP - 315

EP - 323

JO - Metabolic Brain Disease

JF - Metabolic Brain Disease

SN - 0885-7490

IS - 3

ER -

ID: 33505331