Evidence map›Paper›PMID 20801192›Full record

ArticleBiochimica et biophysica acta2010

Hepcidin expression by human monocytes in response to adhesion and pro-inflammatory cytokines.

Xiaolan Zhang, Brad H Rovin

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01726400 (Is Hepcidin a Possible Contributor to Impaired Iron Mobilization and Anaemia in Hepatitis C Patients Treated With Pegylated Interferon Alpha and Ribavirin Therapy? A Pilot Study), which is not on this map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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.

NCT01726400 completednot on this mapstarted 2012, after this paper: background citation

Is Hepcidin a Possible Contributor to Impaired Iron Mobilization and Anaemia in Hepatitis C Patients Treated With Pegylated Interferon Alpha and Ribavirin Therapy? A Pilot Study

TypeobservationalSponsorFremantle Hospital and Health ServiceRan2012 to 2014Enrolled15ConditionsHepatitis CArmsPegylated interferon alpha, Ribavirin
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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  20. Biomarkers and updates on pediatrics lupus nephritis.Rheumatic diseases clinics of North America · 2013
    Review
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

2 authors at 1 institution in 1 country.

Xiaolan ZhangDepartment of Internal Medicine, Ohio State University, Columbus, OH, USA.
Brad H Rovin
The Ohio State University · US

Funding

Modeling SLE Nephritis Through Urine MCP-1R01DK074661 · NIDDK · OHIO STATE UNIVERSITY · PI ROVIN, BRAD H · 2008 to 2010
$669k
Protein Phenotyping of SLE Nephritis Flare CycleR21DK077331 · NIDDK · OHIO STATE UNIVERSITY · PI ROVIN, BRAD H · 2008 to 2009
$413k
NIDDK NIH HHS R01 DK074661NIDDK NIH HHS R21 DK077331NIDDK NIH HHS R21 DK0773311
6 · The paper itself

Abstract

backgroundA previous urine proteomic analysis from our laboratory suggested that hepcidin may be a biomarker for lupus nephritis flare. Immunohistochemical staining of kidney biopsies from lupus patients showed that hepcidin was expressed by infiltrating renal leukocytes. Here we investigated whether inflammatory cytokines relevant to the pathogenesis of lupus nephritis and other glomerular diseases regulate hepcidin expression by human monocytes.

methodsHuman CD14+ monocytes were incubated with interferon alpha (IFNα), interferon gamma (IFNγ), interleukin-6 (IL6), interleukin-1 beta (IL1β), monocyte chemotactic factor-1 (MCP1), or tumor necrosis factor alpha (TNFα). Hepcidin expression was examined by real-time PCR and enzyme immunoassay.

resultsMonocyte hepcidin mRNA increased during adherence to the tissue culture wells, reaching a level 150-fold higher than baseline within 12 h of plating. After accounting for the effects of adhesion, monocytes showed time and dose-dependent up-regulation of hepcidin mRNA upon treatment with IFNα or IL6. One hour of incubation with IFNα or IL6 increased hepcidin mRNA 20 and 80-fold, respectively; by 24 h the mRNA remained 5- and 2.4-fold higher than baseline. IL1β, IFNγ, and MCP-1 did not affect monocyte hepcidin expression. TNFα inhibited hepcidin induction by IL6 in monocytes by 44%. After 24 h of treatment with IFNα or IL6, immunoreactive hepcidin production by monocytes increased 3- and 2.6-fold, respectively.

conclusionHuman monocytes produce hepcidin in response to adhesion and the pro-inflammatory cytokines IFNα and IL6. GENERAL SIGNIFICANCE: The appearance of hepcidin in the kidneys or urine during glomerular diseases may be from infiltrating monocytes induced to express hepcidin by adherence and exposure to pro-inflammatory cytokines found in the renal milieu.

Indexed as

Antimicrobial Cationic PeptidesCell AdhesionChemokine CCL2CytokinesGene ExpressionHepcidinsHep G2 CellsHumansImmunoenzyme TechniquesInflammation MediatorsInterferon-alphaInterferon-gammaInterleukin-1betaInterleukin-6Lipopolysaccharide ReceptorsMonocytesAntimicrobial Cationic PeptidesChemokine CCL2CytokinesHAMP protein, humanHepcidinsInflammation MediatorsInterferon-alphaInterferon-gammaInterleukin-1betaInterleukin-6Lipopolysaccharide ReceptorsRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID20801192
PMCPMC2967603
OpenAlexW2074115660

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Registered trials

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.