Evidence map›Paper›PMID 24556692›Full record

ArticleCell death & disease2014

HMGB1-LPS complex promotes transformation of osteoarthritis synovial fibroblasts to a rheumatoid arthritis synovial fibroblast-like phenotype.

Y Qin, Y Chen, W Wang, Z Wang, G Tang, P Zhang, Z He, Y Liu, S-M Dai, Q Shen

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

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  11. HMGB1 as a therapeutic target in disease.Journal of cellular physiology · 2021
    Review
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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

10 authors at 3 institutions in 1 country.

Y QinDepartment of Laboratory Diagnosis, Changhai Hospital of the Second Military Medical University, Shanghai, China.
Y ChenDepartment of Laboratory Diagnosis, Changhai Hospital of the Second Military Medical University, Shanghai, China.
W WangDepartment of Laboratory Medicine, Xinhua Hospital, Shanghai, China.
Z WangDepartment of Orthopedics, Changhai Hospital of the Second Military Medical University, Shanghai, China.
G TangDepartment of Laboratory Diagnosis, Changhai Hospital of the Second Military Medical University, Shanghai, China.
P ZhangDepartment of Laboratory Diagnosis, Changhai Hospital of the Second Military Medical University, Shanghai, China.
Z HeDepartment of Laboratory Diagnosis, Changhai Hospital of the Second Military Medical University, Shanghai, China.
Y LiuDepartment of Rheumatology and Immunology, Changzheng Hospital of the Second Military Medical University, Shanghai, China.
S-M DaiDepartment of Rheumatology and Immunology, Changhai Hospital of the Second Military Medical University, Shanghai, China.
Q ShenDepartment of Laboratory Diagnosis, Changhai Hospital of the Second Military Medical University, Shanghai, China.
Second Military Medical University · CNChanghai Hospital · CNXinHua Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is generally believed that some inflammatory antigens can recognize Toll-like receptors on synovial fibroblasts (SFs) and then activate downstream signals, leading to the formation of RASFs and inducing rheumatoid arthritis (RA). The objective of the current work was to study on the hypothesis that outer PAMP (LPS) binds to the inner DAMP (HMGB1) and becomes a complex that recognizes TLRs/RAGE on SFs, thus initiating a signaling cascade that leads to the secretion of inflammatory cytokines and chemokines, production of tissue-destructive enzymes, and formation of RASFs, finally resulting in RA. Osteoarthritis synovial fibroblasts (OASFs) were co-cultured with HMGB1-LPS complex in vitro for five generations to induce the transformation of human SFs to RA-like SFs (tOASFs). Then, changes of tOASFs in cell cycle and apoptosis-autophagy balance were investigated in vitro, and the pathogenicity of tOASFs was evaluated in a SCID mouse model in vivo. In vitro cell cycle analysis showed more tOASFs passing through the G1/S checkpoint and moving to S or G2 phase. Flow cytometry and confocal microscopy showed that apoptosis was reduced and autophagy was enhanced significantly in tOASFs as compared with those in OASFs. The expression of certain receptors and adhesion molecules in tOASFs was upregulated. In vivo experiments showed that tOASFs attached to, invaded, and degraded the co-implanted cartilage. In addition, histochemistry showed excessive proliferation of tOASFs and the expression of matrix metalloproteinases (MMPs). Based on the above findings, we conclude that HMGB1-LPS complex could promote the formation of RASFs.

Indexed as

AnimalsApoptosisArthritis, RheumatoidAutophagyCartilageCell AdhesionCell Adhesion MoleculesCell CycleCell DifferentiationCell MovementCell ProliferationCells, CulturedChemokinesCytokinesFibroblastsHMGB1 ProteinCell Adhesion MoleculesChemokinesCytokinesHMGB1 ProteinInflammation MediatorsLipopolysaccharidesMatrix MetalloproteinasesReceptors, Immunologic

Identifiers

PMID24556692
PMCPMC3944262
OpenAlexW2109592369

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.