Evidence map›Paper›PMID 33087182›Full record

ArticleArthritis research & therapy2020

CXCL1 contributes to IL-6 expression in osteoarthritis and rheumatoid arthritis synovial fibroblasts by CXCR2, c-Raf, MAPK, and AP-1 pathway.

Sheng-Mou Hou, Po-Chun Chen, Chieh-Mo Lin, Mei-Ling Fang, Miao-Ching Chi, Ju-Fang Liu

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 64 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

6 authors at 4 institutions in 1 country.

Sheng-Mou HouDepartment of Orthopedic Surgery, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, 111, Taiwan.
Po-Chun ChenTranslational Medicine Center, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, 111, Taiwan.
Chieh-Mo LinDepartment of Nursing, Chang Gung University of Science and Technology, Puzi City, 613, Chiayi County, Taiwan.
Mei-Ling FangCenter for Environmental Toxin and Emerging-Contaminant Research, Cheng Shiu University, Kaohsiung, 833, Taiwan.
Miao-Ching ChiChronic Disease and Health Promotion Research Center, Chang Gung University of Science and Technology, Puzi City, 613, Chiayi County, Taiwan. mcchi@mail.cgust.edu.tw.
Ju-Fang LiuSchool of Oral Hygiene, College of Oral Medicine, Taipei Medical University, No. 250 Wu-Hsing Street, Taipei, 110, Taiwan. jufangliu@tmu.edu.tw.ORCID 0000-0002-0887-6096
Chang Gung University of Science and Technology · TWAsia University · TWCheng Shiu University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteoarthritis (OA) and rheumatoid arthritis (RA) are common joint disorders that are considered to be different diseases due to their unique molecular mechanisms and pathogenesis. Chemokines and their corresponding receptors have been well characterized in RA progression, but less so in OA pathogenesis.

methodsThe human primary synovial fibroblasts (SFs) were obtained from human OA and RA tissue samples. The Western blot and qPCR were performed to analyze the expression levels of CXCL1, as well as CXCL-promoted IL-6 expression in both OASFs and RASFs. The signal cascades that mediate the CXCL1-promoted IL-6 expression were identified by using chemical inhibitors, siRNAs, and shRNAs.

resultsHere, we found that both diseases feature elevated levels of CXCL1 and interleukin (IL)-6, an important proinflammatory cytokine that participates in OA and RA pathogenesis. In OASFs and RASFs, CXCL1 promoted IL-6 expression in a dose- and time-dependent manner. In OASFs and RASFs overexpressing CXCL1 or transduced with shRNA plasmid, IL-6 expression was markedly upregulated. CXCR2, c-Raf, and MAPKs were found to regulate CXCL1-induced IL-6 expression in OASFs and RASFs. Finally, CXCL1 triggered the transcriptional activities of c-Jun (which regulates the expression of proinflammatory proteins) in OASFs and RASFs.

conclusionsOur present work suggests that the CXCL1/CXCR2 axis helps to orchestrate inflammatory responses in OA and RA SFs.

Indexed as

Arthritis, RheumatoidOsteoarthritisCells, CulturedChemokine CXCL1FibroblastsHumansInterleukin-6Synovial MembraneTranscription Factor AP-1Chemokine CXCL1CXCL1 protein, humanInterleukin-6Transcription Factor AP-1CXCL1IL-6OsteoarthritisRheumatoid arthritis

Identifiers

PMID33087182
PMCPMC7580030
OpenAlexW3093796818

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.