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An AKI biomarker lipocalin 2 in the blood derives from the kidney in renal injury but from neutrophils in normal and infected conditions

Standard

An AKI biomarker lipocalin 2 in the blood derives from the kidney in renal injury but from neutrophils in normal and infected conditions. / Kanda, Junya; Mori, Kiyoshi; Kawabata, Hiroshi; Kuwabara, Takashige; Mori, Keita P; Imamaki, Hirotaka; Kasahara, Masato; Yokoi, Hideki; Mizumoto, Chisaki; Thoennissen, Nils H; Koeffler, H Phillip; Barasch, Jonathan; Takaori-Kondo, Akifumi; Mukoyama, Masashi; Nakao, Kazuwa.

in: CLIN EXP NEPHROL, Jahrgang 19, Nr. 1, 06.03.2014, S. 99-106.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Kanda, J, Mori, K, Kawabata, H, Kuwabara, T, Mori, KP, Imamaki, H, Kasahara, M, Yokoi, H, Mizumoto, C, Thoennissen, NH, Koeffler, HP, Barasch, J, Takaori-Kondo, A, Mukoyama, M & Nakao, K 2014, 'An AKI biomarker lipocalin 2 in the blood derives from the kidney in renal injury but from neutrophils in normal and infected conditions', CLIN EXP NEPHROL, Jg. 19, Nr. 1, S. 99-106. https://doi.org/10.1007/s10157-014-0952-7

APA

Kanda, J., Mori, K., Kawabata, H., Kuwabara, T., Mori, K. P., Imamaki, H., Kasahara, M., Yokoi, H., Mizumoto, C., Thoennissen, N. H., Koeffler, H. P., Barasch, J., Takaori-Kondo, A., Mukoyama, M., & Nakao, K. (2014). An AKI biomarker lipocalin 2 in the blood derives from the kidney in renal injury but from neutrophils in normal and infected conditions. CLIN EXP NEPHROL, 19(1), 99-106. https://doi.org/10.1007/s10157-014-0952-7

Vancouver

Kanda J, Mori K, Kawabata H, Kuwabara T, Mori KP, Imamaki H et al. An AKI biomarker lipocalin 2 in the blood derives from the kidney in renal injury but from neutrophils in normal and infected conditions. CLIN EXP NEPHROL. 2014 Mär 6;19(1):99-106. https://doi.org/10.1007/s10157-014-0952-7

Bibtex

@article{f01af7254dc148b0a076e5464a62aa1b,
title = "An AKI biomarker lipocalin 2 in the blood derives from the kidney in renal injury but from neutrophils in normal and infected conditions",
abstract = "BACKGROUND: Lipocalin 2 (LCN2 or neutrophil gelatinase-associated lipocalin) is a secretory protein discovered from neutrophils, which accumulates in the blood and urine during acute kidney injury (AKI) and in the blood by bacterial infection. Little is known about the tissue source and molecular forms of this protein under normal and pathophysiologic conditions.METHODS: By sandwich ELISA, serum and urinary LCN2 levels were measured in 36 patients with hematologic malignancies who transiently became neutropenic by stem cell transplantation (SCT). To evaluate contribution of neutrophil-derived LCN2 in the physiologic blood LCN2 concentrations, we examined CCAAT/enhancer-binding protein ε (C/EBPε) knockout mice, which lack mature neutrophils.RESULTS: In patients without AKI and bacterial infection, at 1 week after SCT, the median blood neutrophil counts became zero and serum LCN2 levels were decreased by 76 ± 6 % (p < 0.01), but urinary LCN2 levels were not altered. During neutropenic conditions, bacterial infection caused only a modest rise of serum LCN2 but AKI produced a marked rise of serum and urinary LCN2 levels. Serum LCN2 concentrations in C/EBPε knockout mice were reduced by 66 ± 11 % compared to wild-type mice (p < 0.05). Blood LCN2 existed predominantly in high molecular weight forms (>100 kDa), while urinary LCN2 was mainly in low molecular weight forms.CONCLUSION: Our findings suggest that neutrophils are the major source of circulating LCN2 in normal and infected conditions, whereas blood and urinary LCN2 mainly derive from the kidney during AKI, and that the molecular forms and regulation of blood and urinary LCN2 are clearly distinct.",
author = "Junya Kanda and Kiyoshi Mori and Hiroshi Kawabata and Takashige Kuwabara and Mori, {Keita P} and Hirotaka Imamaki and Masato Kasahara and Hideki Yokoi and Chisaki Mizumoto and Thoennissen, {Nils H} and Koeffler, {H Phillip} and Jonathan Barasch and Akifumi Takaori-Kondo and Masashi Mukoyama and Kazuwa Nakao",
year = "2014",
month = mar,
day = "6",
doi = "10.1007/s10157-014-0952-7",
language = "English",
volume = "19",
pages = "99--106",
journal = "CLIN EXP NEPHROL",
issn = "1342-1751",
publisher = "Springer Japan",
number = "1",

}

RIS

TY - JOUR

T1 - An AKI biomarker lipocalin 2 in the blood derives from the kidney in renal injury but from neutrophils in normal and infected conditions

AU - Kanda, Junya

AU - Mori, Kiyoshi

AU - Kawabata, Hiroshi

AU - Kuwabara, Takashige

AU - Mori, Keita P

AU - Imamaki, Hirotaka

AU - Kasahara, Masato

AU - Yokoi, Hideki

AU - Mizumoto, Chisaki

AU - Thoennissen, Nils H

AU - Koeffler, H Phillip

AU - Barasch, Jonathan

AU - Takaori-Kondo, Akifumi

AU - Mukoyama, Masashi

AU - Nakao, Kazuwa

PY - 2014/3/6

Y1 - 2014/3/6

N2 - BACKGROUND: Lipocalin 2 (LCN2 or neutrophil gelatinase-associated lipocalin) is a secretory protein discovered from neutrophils, which accumulates in the blood and urine during acute kidney injury (AKI) and in the blood by bacterial infection. Little is known about the tissue source and molecular forms of this protein under normal and pathophysiologic conditions.METHODS: By sandwich ELISA, serum and urinary LCN2 levels were measured in 36 patients with hematologic malignancies who transiently became neutropenic by stem cell transplantation (SCT). To evaluate contribution of neutrophil-derived LCN2 in the physiologic blood LCN2 concentrations, we examined CCAAT/enhancer-binding protein ε (C/EBPε) knockout mice, which lack mature neutrophils.RESULTS: In patients without AKI and bacterial infection, at 1 week after SCT, the median blood neutrophil counts became zero and serum LCN2 levels were decreased by 76 ± 6 % (p < 0.01), but urinary LCN2 levels were not altered. During neutropenic conditions, bacterial infection caused only a modest rise of serum LCN2 but AKI produced a marked rise of serum and urinary LCN2 levels. Serum LCN2 concentrations in C/EBPε knockout mice were reduced by 66 ± 11 % compared to wild-type mice (p < 0.05). Blood LCN2 existed predominantly in high molecular weight forms (>100 kDa), while urinary LCN2 was mainly in low molecular weight forms.CONCLUSION: Our findings suggest that neutrophils are the major source of circulating LCN2 in normal and infected conditions, whereas blood and urinary LCN2 mainly derive from the kidney during AKI, and that the molecular forms and regulation of blood and urinary LCN2 are clearly distinct.

AB - BACKGROUND: Lipocalin 2 (LCN2 or neutrophil gelatinase-associated lipocalin) is a secretory protein discovered from neutrophils, which accumulates in the blood and urine during acute kidney injury (AKI) and in the blood by bacterial infection. Little is known about the tissue source and molecular forms of this protein under normal and pathophysiologic conditions.METHODS: By sandwich ELISA, serum and urinary LCN2 levels were measured in 36 patients with hematologic malignancies who transiently became neutropenic by stem cell transplantation (SCT). To evaluate contribution of neutrophil-derived LCN2 in the physiologic blood LCN2 concentrations, we examined CCAAT/enhancer-binding protein ε (C/EBPε) knockout mice, which lack mature neutrophils.RESULTS: In patients without AKI and bacterial infection, at 1 week after SCT, the median blood neutrophil counts became zero and serum LCN2 levels were decreased by 76 ± 6 % (p < 0.01), but urinary LCN2 levels were not altered. During neutropenic conditions, bacterial infection caused only a modest rise of serum LCN2 but AKI produced a marked rise of serum and urinary LCN2 levels. Serum LCN2 concentrations in C/EBPε knockout mice were reduced by 66 ± 11 % compared to wild-type mice (p < 0.05). Blood LCN2 existed predominantly in high molecular weight forms (>100 kDa), while urinary LCN2 was mainly in low molecular weight forms.CONCLUSION: Our findings suggest that neutrophils are the major source of circulating LCN2 in normal and infected conditions, whereas blood and urinary LCN2 mainly derive from the kidney during AKI, and that the molecular forms and regulation of blood and urinary LCN2 are clearly distinct.

U2 - 10.1007/s10157-014-0952-7

DO - 10.1007/s10157-014-0952-7

M3 - SCORING: Journal article

C2 - 24599361

VL - 19

SP - 99

EP - 106

JO - CLIN EXP NEPHROL

JF - CLIN EXP NEPHROL

SN - 1342-1751

IS - 1

ER -