Evidence map›Paper›PMID 37798786›Full record

ArticleArthritis research & therapy2023

Preosteoclast plays a pathogenic role in syndesmophyte formation of ankylosing spondylitis through the secreted PDGFB - GRB2/ERK/RUNX2 pathway.

Yulong Tang, Kai Yang, Qingmei Liu, Yanyun Ma, Hao Zhu, Kunhai Tang, Chengchun Geng, Jiangnan Xie, Dachun Zhuo, Wenyu Wu and 5 more

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

Article in Arthritis research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.5field-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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
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

15 authors at 4 institutions in 2 countries.

Yulong Tang *State Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-7794-2181
Kai Yang *Department of Dermatology, Jing'an District Central Hospital, Shanghai, China.
Qingmei Liu *Division of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.
Yanyun MaState Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.
Hao ZhuStem Cell Base, Shanghai East Hospital, Shanghai, China.
Kunhai TangState Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0002-2229-6645
Chengchun GengState Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.
Jiangnan XieState Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.
Dachun ZhuoState Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.
Wenyu WuDepartment of Dermatology, Jing'an District Central Hospital, Shanghai, China.
Li JinState Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.
Wenze XiaoDepartment of Rheumatology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China. wenzexiao@fudan.edu.cn.
Jiucun WangState Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China. jcwang@fudan.edu.cn.ORCID http://orcid.org/0000-0003-2765-0620
Qi ZhuInstitute of Arthritis Research, Shanghai Academy of Chinese Medical Sciences, Guanghua Integrative Medicine Hospital, Shanghai, China. zhuqigh540@126.com.
Jing LiuState Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China. liu_jing@fudan.edu.cn.ORCID http://orcid.org/0000-0003-0569-3080
Fudan University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNShanghai East Hospital · CNShanghai Innovative Research Center of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesAnkylosing spondylitis (AS) is a chronic inflammatory disease that mainly affects the sacroiliac joint and spine. However, the real mechanisms of immune cells acting on syndesmophyte formation in AS are not well identified. We aimed to find the key AS-associated cytokine and assess its pathogenic role in AS.

methodsA protein array with 1000 cytokines was performed in five AS patients with the first diagnosis and five age- and gender-matched healthy controls to discover the differentially expressed cytokines. The candidate differentially expressed cytokines were further quantified by multiplex protein quantitation (3 AS-associated cytokines and 3 PDGF-pathway cytokines) and ELISA (PDGFB) in independent samples (a total of 140 AS patients vs 140 healthy controls). The effects of PDGFB, the candidate cytokine, were examined by using adipose-derived stem cells (ADSCs) and human fetal osteoblast cell line (hFOB1.19) as in vitro mesenchymal cell and preosteoblast models, respectively. Furthermore, whole-transcriptome sequencing and enrichment of phosphorylated peptides were performed by using cell models to explore the underlying mechanisms of PDGFB. The xCELLigence system was applied to examine the proliferation, chemotaxis, and migration abilities of PDGFB-stimulated or PDGFB-unstimulated cells.

resultsThe PDGF pathway was observed to have abnormal expression in the protein array, and PDGFB expression was further found to be up-regulated in 140 Chinese AS patients. Importantly, PDGFB expression was significantly correlated with BASFI (Pearson coefficient/p value = 0.62/6.70E - 8) and with the variance of the mSASSS score (mSASSS

conclusionPDGFB stimulates the GRB2/ERK/RUNX2 pathway in ADSCs, promotes osteoblastogenesis of ADSCs, and enhances the extracellular matrix of osteoblasts, which may contribute to pathological bone formation in AS.

Indexed as

Proto-Oncogene Proteins c-sisSpondylitis, AnkylosingCore Binding Factor Alpha 1 SubunitCytokinesGRB2 Adaptor ProteinHumansOsteogenesisSpineCore Binding Factor Alpha 1 SubunitCytokinesGRB2 Adaptor ProteinGRB2 protein, humanProto-Oncogene Proteins c-sisRUNX2 protein, humanAnkylosing spondylitisOsteogenesisPDGFBSyndesmophyte formation

Identifiers

PMID37798786
PMCPMC10552372
OpenAlexW4387370320

What OpenQuestion holds

Textmetadata
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.