Evidence map›Paper›PMID 25349208›Full record

ArticleThe Journal of biological chemistry2014

Differential complement activation pathways promote C3b deposition on native and acetylated LDL thereby inducing lipoprotein binding to the complement receptor 1.

Boudewijn Klop, Pieter van der Pol, Robin van Bruggen, Yanan Wang, Marijke A de Vries, Selvetta van Santen, Joseph O'Flynn, Gert-Jan M van de Geijn, Tjin L Njo, Hans W Janssen and 6 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Trial
  2. Review
  3. Exploring the intersection of atherosclerosis and Alzheimer's disease: the role of inflammation and complement activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  4. Familial Combined Hyperlipidemia: Myth or Reality?Current atherosclerosis reports · 2025
    Review
  5. Review
  6. Article
  7. Article
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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

16 authors at 3 institutions in 1 country.

Boudewijn KlopFrom the Departments of Internal Medicine, Diabetes and Vascular Center.
Pieter van der PolDepartment of Nephrology.
Robin van BruggenSanquin Research, 1006 AN Amsterdam, the Netherlands.
Yanan WangDepartment of Endocrinology and Metabolic Diseases, Einthoven Laboratory for Experimental Vascular Medicine, and.
Marijke A de VriesFrom the Departments of Internal Medicine, Diabetes and Vascular Center.
Selvetta van SantenFrom the Departments of Internal Medicine, Diabetes and Vascular Center.
Joseph O'FlynnDepartment of Nephrology.
Gert-Jan M van de GeijnClinical Chemistry, and.
Tjin L NjoClinical Chemistry, and.
Hans W JanssenClinical Chemistry, and.
Peter de ManMedical Microbiology, Sint Franciscus Gasthuis, 3004 BA Rotterdam, the Netherlands.
J Wouter JukemaDepartment of Cardiology, Leiden University Medical Center, 1006 AN Leiden, the Netherlands, and.
Ton J RabelinkDepartment of Nephrology.
Patrick C N RensenDepartment of Endocrinology and Metabolic Diseases, Einthoven Laboratory for Experimental Vascular Medicine, and.
Cees van KootenDepartment of Nephrology.
Manuel Castro CabezasFrom the Departments of Internal Medicine, Diabetes and Vascular Center, m.castrocabezas@sfg.nl.
Sint Franciscus Gasthuis · NLLeiden University Medical Center · NLSanquin · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipoproteins can induce complement activation resulting in opsonization and binding of these complexes to complement receptors. We investigated the binding of opsonized native LDL and acetylated LDL (acLDL) to the complement receptor 1 (CR1). Binding of complement factors C3b, IgM, C1q, mannose-binding lectin (MBL), and properdin to LDL and acLDL were investigated by ELISA. Subsequent binding of opsonized LDL and acLDL to CR1 on CR1-transfected Chinese Hamster Ovarian cells (CHO-CR1) was tested by flow cytometry. Both native LDL and acLDL induced complement activation with subsequent C3b opsonization upon incubation with normal human serum. Opsonized LDL and acLDL bound to CR1. Binding to CHO-CR1 was reduced by EDTA, whereas MgEGTA only reduced the binding of opsonized LDL, but not of acLDL suggesting involvement of the alternative pathway in the binding of acLDL to CR1. In vitro incubations showed that LDL bound C1q, whereas acLDL bound to C1q, IgM, and properdin. MBL did neither bind to LDL nor to acLDL. The relevance of these findings was demonstrated by the fact that ex vivo up-regulation of CR1 on leukocytes was accompanied by a concomitant increased binding of apolipoprotein B-containing lipoproteins to leukocytes without changes in LDL-receptor expression. In conclusion, CR1 is able to bind opsonized native LDL and acLDL. Binding of LDL to CR1 is mediated via the classical pathway, whereas binding of acLDL is mediated via both the classical and alternative pathways. Binding of lipoproteins to CR1 may be of clinical relevance due to the ubiquitous cellular distribution of CR1.

Indexed as

Complement ActivationAnimalsApolipoproteins BCells, CulturedCHO CellsComplement C1qComplement C3bComplement Pathway, AlternativeComplement Pathway, ClassicalCricetinaeCricetulusEdetic AcidFlow CytometryHumansImmunoglobulin MLeukocytesacetyl-LDLApolipoproteins BComplement C1qComplement C3bEdetic AcidImmunoglobulin MLipopolysaccharidesLipoproteins, LDLOpsonin ProteinsProperdinReceptors, Complement 3bC3bComplementComplement ActivationCR1ErythrocyteLeukocyteLipoproteinLow-density Lipoprotein (LDL)Receptor

Identifiers

PMID25349208
PMCPMC4271227
OpenAlexW2020797304

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.