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Title: An AKI biomarker lipocalin 2 in the blood derives from the kidney in renal injury but from neutrophils in normal and infected conditions.
Authors: Kanda, Junya  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-6704-3633 (unconfirmed)
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
Author's alias: 森, 潔
Keywords: Acute kidney injury
Neutrophil
Sepsis, bone marrow transplantation
Biomarker
Issue Date: Feb-2015
Publisher: Springer Japan
Journal title: Clinical and experimental nephrology
Volume: 19
Issue: 1
Start page: 99
End page: 106
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.
Description: First online: 06 March 2014
Rights: The final publication is available at Springer via http://dx.doi.org/10.1007/s10157-014-0952-7.
The full-text file will be made open to the public on 06 March 2015 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。This is not the published version. Please cite only the published version.
URI: http://hdl.handle.net/2433/202580
DOI(Published Version): 10.1007/s10157-014-0952-7
PubMed ID: 24599361
Appears in Collections:Journal Articles

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