Evidence map›Paper›PMID 29070980›Full record

ArticleTransfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie2017

Components in Plasma-Derived Factor VIII, But Not in Recombinant Factor VIII Downregulate Anti-Inflammatory Surface Marker CD163 in Human Macrophages through Release of CXCL4 (Platelet Factor 4).

Anne Bertling, Martin F Brodde, Mayken Visser, Janina Treffon, Michelle Fennen, Anke C Fender, Reinhard Kelsch, Beate E Kehrel

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 92% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

8 authors at 3 institutions in 1 country.

Anne BertlingDepartment of Anesthesiology, Intensive Care and Pain Medicine, Experimental and Clinical Hemostasis, University of Münster, Münster, Germany.
Martin F BroddeDepartment of Anesthesiology, Intensive Care and Pain Medicine, Experimental and Clinical Hemostasis, University of Münster, Münster, Germany.
Mayken VisserDepartment of Anesthesiology, Intensive Care and Pain Medicine, Experimental and Clinical Hemostasis, University of Münster, Münster, Germany.
Janina TreffonDepartment of Anesthesiology, Intensive Care and Pain Medicine, Experimental and Clinical Hemostasis, University of Münster, Münster, Germany.
Michelle FennenDepartment of Anesthesiology, Intensive Care and Pain Medicine, Experimental and Clinical Hemostasis, University of Münster, Münster, Germany.
Anke C FenderInstitute of Pharmacology and Clinical Pharmacology, Heinrich-Heine-University, Düsseldorf, Germany.
Reinhard KelschInstitute of Transfusion Medicine and Transplantation Immunology, University Hospital Münster, Münster, Germany.
Beate E KehrelDepartment of Anesthesiology, Intensive Care and Pain Medicine, Experimental and Clinical Hemostasis, University of Münster, Münster, Germany.
University of Münster · DEHeinrich Heine University Düsseldorf · DEUniversity Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHemarthrosis, or bleeding into the joints, is a hallmark of hemophilia. Heme triggers oxidative stress, inflammation, and destruction of cartilage and bone. The haptoglobin-CD163-heme oxygenase-1 (HO-1) pathway circumvents heme toxicity through enzymatic degradation of heme and transcription of antioxidant genes. Plasma-derived factor concentrates contain many proteins that might impact on cellular pathways in joints, blood, and vessels.

methodsActivation of platelets from healthy volunteers was assessed by flow cytometry analysis of fibrinogen binding and CD62P expression. Platelet CXCL4 release was measured by ELISA. Human peripheral blood mononuclear cells were exposed to CXCL4 or platelet supernatants (untreated or pre-stimulated with factor VIII (FVIII) products) during their differentiation to macrophages and analyzed for CD163 expression. Some macrophage cultures were additionally incubated with autologous hemoglobin for 18 h for analysis of HO-1 expression.

resultsPlatelet CXCL4 release was increased by all 8 tested plasma-derived FVIII products but not the 3 recombinant products. Macrophages exposed to supernatant from platelets treated with some plasma-derived FVIII products downregulated CD163 surface expression and failed to upregulate the athero- and joint protective enzyme HO-1 in response to hemoglobin.

conclusionPlasma-derived FVIII products might promote bleeding-induced joint injury via generation of macrophages that are unable to counteract redox stress.

Indexed as

Factor VIIIHemophilia AMacrophagesPlateletsScavenger receptors

Identifiers

PMID29070980
PMCPMC5649264
OpenAlexW2743471736

What OpenQuestion holds

Textmetadata
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.