Evidence map›Paper›PMID 23028973›Full record

ArticlePloS one2012

Role of macrophage CCAAT/enhancer binding protein delta in the pathogenesis of rheumatoid arthritis in collagen-induced arthritic mice.

Ling-Hua Chang, Huei-Sheng Huang, Po-Ting Wu, I-Ming Jou, Min-Hsiung Pan, Wen-Chang Chang, Dennis Ding Hwa Wang, Ju-Ming Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 9% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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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 5 institutions in 2 countries.

Ling-Hua ChangInstitute of Basic Medical Sciences, College of Medicine, Tainan, Taiwan.
Huei-Sheng Huang
Po-Ting Wu
I-Ming Jou
Min-Hsiung Pan
Wen-Chang Chang
Dennis Ding Hwa Wang
Ju-Ming Wang
Institute of Basic Medical Sciences of the Chinese Academy of Medical SciencesNational Cheng Kung University Hospital · TWTaipei Medical University · TWNational Kaohsiung Marine University · TWUniversity of California, Irvine · US

Funding

BLRD VA IK2 BX006111
6 · The paper itself

Abstract

backgroundThe up-regulation of CCAAT/enhancer binding protein delta (CEBPD) has frequently been observed in macrophages in age-associated disorders, including rheumatoid arthritis (RA). However, the role of macrophage CEBPD in the pathogenesis of RA is unclear. METHODOLOGY AND PRINCIPAL

findingsWe found that the collagen-induced arthritis (CIA) score and the number of affected paws in Cebpd(-/-) mice were significantly decreased compared with the wild-type (WT) mice. The histological analysis revealed an attenuated CIA in Cebpd(-/-) mice, as shown by reduced pannus formation and greater integrity of joint architecture in affected paws of Cebpd(-/-) mice compared with WT mice. In addition, immunohistochemistry analysis revealed decreased pannus proliferation and angiogenesis in Cebpd(-/-) mice compared with WT mice. CEBPD activated in macrophages played a functional role in promoting the tube formation of endothelial cells and the migration and proliferation of synoviocytes. In vivo DNA binding assays and reporter assays showed that CEBPD up-regulated CCL20, CXCL1, IL23A and TNFAIP6 transcripts through direct binding to their promoter regions. CCL20, IL23A, CXCL1 and TNFAIP6 contributed to the migration and proliferation of synoviocytes, and the latter two proteins were involved in tube formation of endothelial cells. Finally, two anti-inflammatory chemicals, inotilone and rosmanol, reduced the expression of CEBPD and its downstream targets and mitigated the above phenomena. CONCLUSIONS AND SIGNIFICANCE: Collectively, our findings suggest that CEBPD and its downstream effectors could be biomarkers for the diagnosis of RA and potentially serve as therapeutic targets for RA therapy.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidCCAAT-Enhancer-Binding Protein-deltaCell Adhesion MoleculesCell LineCell Line, TumorCell MovementCell ProliferationCells, CulturedChemokine CCL20Chemokine CXCL1Chromatin ImmunoprecipitationHumansInterleukin-23 Subunit p19MiceCCAAT-Enhancer-Binding Protein-deltaCell Adhesion MoleculesChemokine CCL20Chemokine CXCL1Il23a protein, mouseInterleukin-23 Subunit p19Tnfaip6 protein, mouse

Identifiers

PMID23028973
PMCPMC3454428
OpenAlexW2022149910

What OpenQuestion holds

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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.