Evidence map›Paper›PMID 24124495›Full record

ArticlePloS one2013

Improved mass spectrometry assay for plasma hepcidin: detection and characterization of a novel hepcidin isoform.

Coby M M Laarakkers, Erwin T Wiegerinck, Siem Klaver, Maria Kolodziejczyk, Hendrik Gille, Andreas M Hohlbaum, Harold Tjalsma, Dorine W Swinkels

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
6.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 85 citations in OpenAlex.

  1. Trial
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  9. Hepcidin as a Potential Biomarker for the Diagnosis of Anemia.Turkish journal of pharmaceutical sciences · 2022
    Article
  10. Clinical interpretation of serum hepcidin-25 in inflammation and renal dysfunction.Journal of mass spectrometry and advances in the clinical lab · 2022
    Article
  11. Transferrin Saturation/Hepcidin Ratio DiscriminatesInternational journal of molecular sciences · 2022
    Article
  12. Article
  13. Article
  14. Observational
  15. Article
  16. Article
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  19. New diagnostic tools for delineating iron status.Hematology. American Society of Hematology. Education Program · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Coby M M LaarakkersLaboratory of Genetic, Endocrine and Metabolic Diseases, Department of Laboratory Medicine, Radboud University Medical Centre, Nijmegen, The Netherlands ; Hepcidinanalysis.com, Nijmegen, The Netherlands.
Erwin T Wiegerinck
Siem Klaver
Maria Kolodziejczyk
Hendrik Gille
Andreas M Hohlbaum
Harold Tjalsma
Dorine W Swinkels
Radboud University Medical Center · NLRadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mass spectrometry (MS)-based assays for the quantification of the iron regulatory hormone hepcidin are pivotal to discriminate between the bioactive 25-amino acid form that can effectively block the sole iron transporter ferroportin and other naturally occurring smaller isoforms without a known role in iron metabolism. Here we describe the design, validation and use of a novel stable hepcidin-25(+40) isotope as internal standard for quantification. Importantly, the relative large mass shift of 40 Da makes this isotope also suitable for easy-to-use medium resolution linear time-of-flight (TOF) platforms. As expected, implementation of hepcidin-25(+40) as internal standard in our weak cation exchange (WCX) TOF MS method yielded very low inter/intra run coefficients of variation. Surprisingly, however, in samples from kidney disease patients, we detected a novel peak (m/z 2673.9) with low intensity that could be identified as hepcidin-24 and had previously remained unnoticed due to peak interference with the formerly used internal standard. Using a cell-based bioassay it was shown that synthetic hepcidin-24 was, like the -22 and -20 isoforms, a significantly less potent inducer of ferroportin degradation than hepcidin-25. During prolonged storage of plasma at room temperature, we observed that a decrease in plasma hepcidin-25 was paralleled by an increase in the levels of the hepcidin-24, -22 and -20 isoforms. This provides first evidence that all determinants for the conversion of hepcidin-25 to smaller inactive isoforms are present in the circulation, which may contribute to the functional suppression of hepcidin-25, that is significantly elevated in patients with renal impairment. The present update of our hepcidin TOF MS assay together with improved insights in the source and preparation of the internal standard, and sample stability will further improve our understanding of circulating hepcidin and pave the way towards further optimization and standardization of plasma hepcidin assays.

Indexed as

HepcidinsHumansMass SpectrometryProtein IsoformsReproducibility of ResultsSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationHepcidinsProtein Isoforms

Identifiers

PMID24124495
PMCPMC3790851
OpenAlexW1993415721

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.