Evidence map›Paper›PMID 31777818›Full record

ArticleACR open rheumatology2019

Binding Immunoglobulin Protein (BIP) Inhibits TNF-α-Induced Osteoclast Differentiation and Systemic Bone Loss in an Erosive Arthritis Model.

Mario M Zaiss, Christopher Hall, Neil W A McGowan, Rebecca Babb, Vikesh Devlia, Sébastien Lucas, Sajeda Meghji, Brian Henderson, Aline Bozec, Georg Schett and 4 more

Open access · goldAbstract read
In one paragraph

Article in ACR open rheumatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

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  11. The M-CSF receptor in osteoclasts and beyond.Experimental & molecular medicine · 2020
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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

14 authors at 4 institutions in 2 countries.

Mario M ZaissFriedrich-Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen Erlangen Germany.
Christopher HallKing's College London London UK.ORCID https://orcid.org/0000-0001-6156-4975
Neil W A McGowanKing's College London London UK.
Rebecca BabbKing's College London London UK.
Vikesh DevliaKing's College London London UK.
Sébastien LucasFriedrich-Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen Erlangen Germany.
Sajeda MeghjiUCL-Eastman Dental Institute University College London London UK.
Brian HendersonUCL-Eastman Dental Institute University College London London UK.
Aline BozecFriedrich-Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen Erlangen Germany.
Georg SchettFriedrich-Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen Erlangen Germany.
Jean-Pierre DavidFriedrich-Alexander University Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, Erlangen, Germany, and Institute of Osteology and Biomechanics (IOBM) University Medical Center Hamburg-Eppendorf Hamburg Germany.
Gabriel S PanayiKing's College London London UK.
Agamemnon E GrigoriadisKing's College London London UK.ORCID https://orcid.org/0000-0002-5941-8132
Valerie M CorrigallKing's College London London UK.
King's College London · GBFriedrich-Alexander-Universität Erlangen-Nürnberg · DEEastman Dental Hospital · GBUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe association between inflammation and dysregulated bone remodeling is apparent in rheumatoid arthritis and is recapitulated in the human tumor necrosis factor transgenic (

methods

resultsBiP-treated mice showed reduced inflammation and cartilage destruction, and histomorphometric analysis revealed a decrease in osteoclast number with protection from systemic bone loss. Abrogation of osteoclast function was also observed in an ex vivo murine calvarial model. BiP inhibited differentiation of osteoclast precursors and prevented bone resorption by mature osteoclasts in vitro. BiP also induced downregulation of CD115/c-Fms and Receptor Activator of NF-κB (RANK) messenger RNA and protein, causing reduced phosphorylation of the p38 mitogen-activated protein kinases, extracellular signal-regulated kinases 1/2 and p38, with suppression of essential osteoclast transcription factors, c-Fos and NFATc1. BiP directly inhibited TNF-α- or Receptor Activator of NF-κB Ligand (RANKL)-induced NF-κB nuclear translocation in THP-1 monocytic cells and preosteoclasts by the canonical and noncanonical pathways.

conclusionBiP combines an anti-inflammatory function with antiosteoclast activity, which establishes it as a potential novel therapeutic for inflammatory disorders associated with bone loss.

Identifiers

PMID31777818
PMCPMC6857990
OpenAlexW2965456192

What OpenQuestion holds

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LicenceCC BY
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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.