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High phosphate directly affects endothelial function by downregulating annexin II

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High phosphate directly affects endothelial function by downregulating annexin II. / Di Marco, Giovana Seno; König, Maximilian; Stock, Christian; Wiesinger, Anne; Hillebrand, Uta; Reiermann, Stefanie; Reuter, Stefan; Amler, Susanne; Köhler, Gabriele; Buck, Friedrich; Fobker, Manfred; Kümpers, Philipp; Oberleithner, Hans; Hausberg, Martin; Lang, Detlef; Pavenstädt, Hermann; Brand, Marcus.

In: KIDNEY INT, Vol. 83, No. 2, 01.02.2013, p. 213-22.

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

Harvard

Di Marco, GS, König, M, Stock, C, Wiesinger, A, Hillebrand, U, Reiermann, S, Reuter, S, Amler, S, Köhler, G, Buck, F, Fobker, M, Kümpers, P, Oberleithner, H, Hausberg, M, Lang, D, Pavenstädt, H & Brand, M 2013, 'High phosphate directly affects endothelial function by downregulating annexin II', KIDNEY INT, vol. 83, no. 2, pp. 213-22. https://doi.org/10.1038/ki.2012.300

APA

Di Marco, G. S., König, M., Stock, C., Wiesinger, A., Hillebrand, U., Reiermann, S., Reuter, S., Amler, S., Köhler, G., Buck, F., Fobker, M., Kümpers, P., Oberleithner, H., Hausberg, M., Lang, D., Pavenstädt, H., & Brand, M. (2013). High phosphate directly affects endothelial function by downregulating annexin II. KIDNEY INT, 83(2), 213-22. https://doi.org/10.1038/ki.2012.300

Vancouver

Di Marco GS, König M, Stock C, Wiesinger A, Hillebrand U, Reiermann S et al. High phosphate directly affects endothelial function by downregulating annexin II. KIDNEY INT. 2013 Feb 1;83(2):213-22. https://doi.org/10.1038/ki.2012.300

Bibtex

@article{3c2edfdf5cfc43518ccd26037257eca1,
title = "High phosphate directly affects endothelial function by downregulating annexin II",
abstract = "Hyperphosphatemia is associated with increased cardiovascular risk in patients with renal disease and in healthy individuals. Here we tested whether high phosphate has a role in the pathophysiology of cardiovascular events by interfering with endothelial function, thereby impairing microvascular function and angiogenesis. Protein expression analysis found downregulation of annexin II in human coronary artery endothelial cells, an effect associated with exacerbated shedding of annexin II-positive microparticles by the cells exposed to high phosphate media. EAhy926 endothelial cells exposed to sera from hyperphosphatemic patients also display decreased annexin II, suggesting a negative correlation between serum phosphate and annexin II expression. By using endothelial cell-based assays in vitro and the chicken chorioallantoic membrane assay in vivo, we found that angiogenesis, vessel wall morphology, endothelial cell migration, capillary tube formation, and endothelial survival were impaired in a hyperphosphatemic milieu. Blockade of membrane-bound extracellular annexin II with a specific antibody mimicked the effects of high phosphate. In addition, high phosphate stiffened endothelial cells in vitro and in rats in vivo. Thus, our results link phosphate and adverse clinical outcomes involving the endothelium in both healthy individuals and patients with renal disease.",
keywords = "Animals, Annexin A2, Apoptosis, Cell Movement, Cells, Cultured, Chick Embryo, Down-Regulation, Humans, Hyperphosphatemia, Male, Neovascularization, Physiologic, Proteomics, Rats, Rats, Sprague-Dawley, Renal Insufficiency, Chronic, Vascular Stiffness",
author = "{Di Marco}, {Giovana Seno} and Maximilian K{\"o}nig and Christian Stock and Anne Wiesinger and Uta Hillebrand and Stefanie Reiermann and Stefan Reuter and Susanne Amler and Gabriele K{\"o}hler and Friedrich Buck and Manfred Fobker and Philipp K{\"u}mpers and Hans Oberleithner and Martin Hausberg and Detlef Lang and Hermann Pavenst{\"a}dt and Marcus Brand",
year = "2013",
month = feb,
day = "1",
doi = "10.1038/ki.2012.300",
language = "English",
volume = "83",
pages = "213--22",
journal = "KIDNEY INT",
issn = "0085-2538",
publisher = "NATURE PUBLISHING GROUP",
number = "2",

}

RIS

TY - JOUR

T1 - High phosphate directly affects endothelial function by downregulating annexin II

AU - Di Marco, Giovana Seno

AU - König, Maximilian

AU - Stock, Christian

AU - Wiesinger, Anne

AU - Hillebrand, Uta

AU - Reiermann, Stefanie

AU - Reuter, Stefan

AU - Amler, Susanne

AU - Köhler, Gabriele

AU - Buck, Friedrich

AU - Fobker, Manfred

AU - Kümpers, Philipp

AU - Oberleithner, Hans

AU - Hausberg, Martin

AU - Lang, Detlef

AU - Pavenstädt, Hermann

AU - Brand, Marcus

PY - 2013/2/1

Y1 - 2013/2/1

N2 - Hyperphosphatemia is associated with increased cardiovascular risk in patients with renal disease and in healthy individuals. Here we tested whether high phosphate has a role in the pathophysiology of cardiovascular events by interfering with endothelial function, thereby impairing microvascular function and angiogenesis. Protein expression analysis found downregulation of annexin II in human coronary artery endothelial cells, an effect associated with exacerbated shedding of annexin II-positive microparticles by the cells exposed to high phosphate media. EAhy926 endothelial cells exposed to sera from hyperphosphatemic patients also display decreased annexin II, suggesting a negative correlation between serum phosphate and annexin II expression. By using endothelial cell-based assays in vitro and the chicken chorioallantoic membrane assay in vivo, we found that angiogenesis, vessel wall morphology, endothelial cell migration, capillary tube formation, and endothelial survival were impaired in a hyperphosphatemic milieu. Blockade of membrane-bound extracellular annexin II with a specific antibody mimicked the effects of high phosphate. In addition, high phosphate stiffened endothelial cells in vitro and in rats in vivo. Thus, our results link phosphate and adverse clinical outcomes involving the endothelium in both healthy individuals and patients with renal disease.

AB - Hyperphosphatemia is associated with increased cardiovascular risk in patients with renal disease and in healthy individuals. Here we tested whether high phosphate has a role in the pathophysiology of cardiovascular events by interfering with endothelial function, thereby impairing microvascular function and angiogenesis. Protein expression analysis found downregulation of annexin II in human coronary artery endothelial cells, an effect associated with exacerbated shedding of annexin II-positive microparticles by the cells exposed to high phosphate media. EAhy926 endothelial cells exposed to sera from hyperphosphatemic patients also display decreased annexin II, suggesting a negative correlation between serum phosphate and annexin II expression. By using endothelial cell-based assays in vitro and the chicken chorioallantoic membrane assay in vivo, we found that angiogenesis, vessel wall morphology, endothelial cell migration, capillary tube formation, and endothelial survival were impaired in a hyperphosphatemic milieu. Blockade of membrane-bound extracellular annexin II with a specific antibody mimicked the effects of high phosphate. In addition, high phosphate stiffened endothelial cells in vitro and in rats in vivo. Thus, our results link phosphate and adverse clinical outcomes involving the endothelium in both healthy individuals and patients with renal disease.

KW - Animals

KW - Annexin A2

KW - Apoptosis

KW - Cell Movement

KW - Cells, Cultured

KW - Chick Embryo

KW - Down-Regulation

KW - Humans

KW - Hyperphosphatemia

KW - Male

KW - Neovascularization, Physiologic

KW - Proteomics

KW - Rats

KW - Rats, Sprague-Dawley

KW - Renal Insufficiency, Chronic

KW - Vascular Stiffness

U2 - 10.1038/ki.2012.300

DO - 10.1038/ki.2012.300

M3 - SCORING: Journal article

C2 - 22913982

VL - 83

SP - 213

EP - 222

JO - KIDNEY INT

JF - KIDNEY INT

SN - 0085-2538

IS - 2

ER -