Evidence map›Paper›PMID 33297736›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2021

FOXM1 activates JAK1/STAT3 pathway in human osteoarthritis cartilage cell inflammatory reaction.

Runming Zeng, Xiaohui Lu, Jing Lin, Zhijie Ron, Jiezhuang Fang, Zewa Liu, Wanting Zeng

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

Article in Experimental biology and medicine (Maywood, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 32 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

7 authors at 2 institutions in 2 countries.

Runming ZengDepartment of Orthopedic Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, China.ORCID 0000-0002-8990-4377
Xiaohui LuDepartment of Orthopedic Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, China.
Jing LinDepartment of Oncology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, China.
Zhijie RonDepartment of Orthopedic Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, China.
Jiezhuang FangDepartment of Orthopedic Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, China.
Zewa LiuDepartment of Oncology, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, China.
Wanting ZengDivision of Medicine, University College London, London WC1E 6BT, UK.
Shantou University · CNUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA), the most prevalent form of arthritis disease, is characterized by destruction of articular cartilage, osteophyte development, and sclerosis of subchondral bone. Transcription factors Janus kinase 1/signal transducer and activator of transcription 3 (JAK1/STAT3) and Forkhead box M1 (FOXM1) are key mediators of this inflammatory reaction. In this study, we investigated the interaction between JAK1/STAT3 and FOXM1 in OA. Inflammation is related to the cartilage damage, and lipopolysaccharides (LPS) are a major pro-inflammatory inducer, so LPS was utilized to stimulate chondrocytes and establish a cell-based OA model. We found LPS treatment caused a generation of inflammatory cell factors (IL-1β, IL-6, and TNF-α), and upregulation of inducible nitric oxide synthases (iNOS), cyclooxygenase-2 (COX-2), nitric oxide (NO), prostaglandin E2 (PGE2) and other inflammatory mediators. Cell viability of chondrocytes was impaired with LPS stimulation, along with an upregulation of JAK1 expression, and phosphorylation and nuclear accumulation of STAT3. The administration of STAT3 inhibitor WP1066, which abated activation and nuclear location of STAT3, depleted the effect of LPS on inflammation and cell death. Co-immunoprecipitation showed that STAT3 was able to bind to FOXM1, and deactivation of STAT3 resulted in the downregulation of FOXM1. Moreover, FOXM1 silencing inhibited the generation of inflammatory cytokines induced by LPS, and the attenuation of cell survival. These findings indicated that the interaction between JAK1/STAT3 and FOXM1 may play a key role in OA pathogenic studies, and suggest the JAK1/STAT3 pathway may be a potential target for OA therapy.

Indexed as

Signal TransductionCartilage, ArticularCells, CulturedChondrocytesForkhead Box Protein M1Gene SilencingHumansInflammationJanus Kinase 1LipopolysaccharidesOsteoarthritisPhosphorylationProtein BindingPyridinesPyrrolesSTAT3 Transcription Factor4-(5-(cyclopropylcarbamoyl)-2-methylphenylamino)-5-methyl-N-propylpyrrolo(1,2-f)(1,2,4)triazine-6-carboxamideForkhead Box Protein M1FOXM1 protein, humanJanus Kinase 1LipopolysaccharidesPyridinesPyrrolesSTAT3 Transcription FactorTriazinesTyrphostinsWP1066chondrocytesFOXM1inflammationJAK1lipopolysaccharidesOsteoarthritisSTAT3

Identifiers

PMID33297736
PMCPMC7988721
OpenAlexW3112263917

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.