Effects of apolipoprotein M in uremic atherosclerosis

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Effects of apolipoprotein M in uremic atherosclerosis. / Bosteen, Markus Høybye; Madsen Svarrer, Eva Martha; Bisgaard, Line Stattau; Martinussen, Torben; Madsen, Marie; Nielsen, Lars Bo; Christoffersen, Christina; Pedersen, Tanja Xenia.

I: Atherosclerosis, Bind 265, 10.2017, s. 93-101.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Bosteen, MH, Madsen Svarrer, EM, Bisgaard, LS, Martinussen, T, Madsen, M, Nielsen, LB, Christoffersen, C & Pedersen, TX 2017, 'Effects of apolipoprotein M in uremic atherosclerosis', Atherosclerosis, bind 265, s. 93-101. https://doi.org/10.1016/j.atherosclerosis.2017.08.005

APA

Bosteen, M. H., Madsen Svarrer, E. M., Bisgaard, L. S., Martinussen, T., Madsen, M., Nielsen, L. B., Christoffersen, C., & Pedersen, T. X. (2017). Effects of apolipoprotein M in uremic atherosclerosis. Atherosclerosis, 265, 93-101. https://doi.org/10.1016/j.atherosclerosis.2017.08.005

Vancouver

Bosteen MH, Madsen Svarrer EM, Bisgaard LS, Martinussen T, Madsen M, Nielsen LB o.a. Effects of apolipoprotein M in uremic atherosclerosis. Atherosclerosis. 2017 okt;265:93-101. https://doi.org/10.1016/j.atherosclerosis.2017.08.005

Author

Bosteen, Markus Høybye ; Madsen Svarrer, Eva Martha ; Bisgaard, Line Stattau ; Martinussen, Torben ; Madsen, Marie ; Nielsen, Lars Bo ; Christoffersen, Christina ; Pedersen, Tanja Xenia. / Effects of apolipoprotein M in uremic atherosclerosis. I: Atherosclerosis. 2017 ; Bind 265. s. 93-101.

Bibtex

@article{96f8e99763b549ccabc6242486419db3,
title = "Effects of apolipoprotein M in uremic atherosclerosis",
abstract = "BACKGROUND AND AIMS: Chronic kidney disease is characterized by uremia and causes premature death, partly due to accelerated atherosclerosis. Apolipoprotein (apo) M is a plasma carrier protein for the lipid sphingosine-1-phosphate (S1P). The Apom-S1P complex associates with HDL, and may contribute to its anti-atherosclerotic effects. The role of Apom/S1P in atherosclerosis is presently controversial and has not been explored in a uremic setting. We aimed to explore whether plasma concentrations of Apom/S1P are altered by uremia and whether Apom overexpression or deficiency affects classical and uremic atherosclerosis.METHODS: Mild to moderate uremia was induced by subtotal nephrectomy (NX) in 86-92 Apoe-deficient mice that were either Apom-wild type, Apom-deficient, or overexpressed Apom (∼10 fold). The effects of uremia on plasma Apom/S1P and atherosclerosis were evaluated and compared to non-nephrectomized controls.RESULTS: Uremia increased plasma Apom by ∼25%, but not S1P. Plasma S1P was elevated by ∼300% in mice overexpressing Apom, and decreased by ∼25% in Apom-deficient mice. Apom overexpression augmented aortic root atherosclerosis and plasma cholesterol. In contrast, aortic arch atherosclerosis was unaffected by the Apom genotype. There was no effect of Apom-deficiency or Apom overexpression on uremic atherosclerosis.CONCLUSIONS: This study highlights the complexity of Apom/S1P in atherosclerosis and challenges the notion that the Apom/S1P complex is anti-atherogenic, at least in Apoe-deficient mice.",
author = "Bosteen, {Markus H{\o}ybye} and {Madsen Svarrer}, {Eva Martha} and Bisgaard, {Line Stattau} and Torben Martinussen and Marie Madsen and Nielsen, {Lars Bo} and Christina Christoffersen and Pedersen, {Tanja Xenia}",
note = "Copyright {\textcopyright} 2017 Elsevier B.V. All rights reserved.",
year = "2017",
month = oct,
doi = "10.1016/j.atherosclerosis.2017.08.005",
language = "English",
volume = "265",
pages = "93--101",
journal = "Atherosclerosis",
issn = "0021-9150",
publisher = "Elsevier Ireland Ltd",

}

RIS

TY - JOUR

T1 - Effects of apolipoprotein M in uremic atherosclerosis

AU - Bosteen, Markus Høybye

AU - Madsen Svarrer, Eva Martha

AU - Bisgaard, Line Stattau

AU - Martinussen, Torben

AU - Madsen, Marie

AU - Nielsen, Lars Bo

AU - Christoffersen, Christina

AU - Pedersen, Tanja Xenia

N1 - Copyright © 2017 Elsevier B.V. All rights reserved.

PY - 2017/10

Y1 - 2017/10

N2 - BACKGROUND AND AIMS: Chronic kidney disease is characterized by uremia and causes premature death, partly due to accelerated atherosclerosis. Apolipoprotein (apo) M is a plasma carrier protein for the lipid sphingosine-1-phosphate (S1P). The Apom-S1P complex associates with HDL, and may contribute to its anti-atherosclerotic effects. The role of Apom/S1P in atherosclerosis is presently controversial and has not been explored in a uremic setting. We aimed to explore whether plasma concentrations of Apom/S1P are altered by uremia and whether Apom overexpression or deficiency affects classical and uremic atherosclerosis.METHODS: Mild to moderate uremia was induced by subtotal nephrectomy (NX) in 86-92 Apoe-deficient mice that were either Apom-wild type, Apom-deficient, or overexpressed Apom (∼10 fold). The effects of uremia on plasma Apom/S1P and atherosclerosis were evaluated and compared to non-nephrectomized controls.RESULTS: Uremia increased plasma Apom by ∼25%, but not S1P. Plasma S1P was elevated by ∼300% in mice overexpressing Apom, and decreased by ∼25% in Apom-deficient mice. Apom overexpression augmented aortic root atherosclerosis and plasma cholesterol. In contrast, aortic arch atherosclerosis was unaffected by the Apom genotype. There was no effect of Apom-deficiency or Apom overexpression on uremic atherosclerosis.CONCLUSIONS: This study highlights the complexity of Apom/S1P in atherosclerosis and challenges the notion that the Apom/S1P complex is anti-atherogenic, at least in Apoe-deficient mice.

AB - BACKGROUND AND AIMS: Chronic kidney disease is characterized by uremia and causes premature death, partly due to accelerated atherosclerosis. Apolipoprotein (apo) M is a plasma carrier protein for the lipid sphingosine-1-phosphate (S1P). The Apom-S1P complex associates with HDL, and may contribute to its anti-atherosclerotic effects. The role of Apom/S1P in atherosclerosis is presently controversial and has not been explored in a uremic setting. We aimed to explore whether plasma concentrations of Apom/S1P are altered by uremia and whether Apom overexpression or deficiency affects classical and uremic atherosclerosis.METHODS: Mild to moderate uremia was induced by subtotal nephrectomy (NX) in 86-92 Apoe-deficient mice that were either Apom-wild type, Apom-deficient, or overexpressed Apom (∼10 fold). The effects of uremia on plasma Apom/S1P and atherosclerosis were evaluated and compared to non-nephrectomized controls.RESULTS: Uremia increased plasma Apom by ∼25%, but not S1P. Plasma S1P was elevated by ∼300% in mice overexpressing Apom, and decreased by ∼25% in Apom-deficient mice. Apom overexpression augmented aortic root atherosclerosis and plasma cholesterol. In contrast, aortic arch atherosclerosis was unaffected by the Apom genotype. There was no effect of Apom-deficiency or Apom overexpression on uremic atherosclerosis.CONCLUSIONS: This study highlights the complexity of Apom/S1P in atherosclerosis and challenges the notion that the Apom/S1P complex is anti-atherogenic, at least in Apoe-deficient mice.

U2 - 10.1016/j.atherosclerosis.2017.08.005

DO - 10.1016/j.atherosclerosis.2017.08.005

M3 - Journal article

C2 - 28866363

VL - 265

SP - 93

EP - 101

JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

ER -

ID: 183469868