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


Journal

Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438

Informations de publication

Date de publication:
05 10 2023
Historique:
received: 14 11 2022
accepted: 21 08 2023
medline: 9 10 2023
pubmed: 6 10 2023
entrez: 5 10 2023
Statut: epublish

Résumé

Ankylosing 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. A 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. The 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 PDGFB 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.

Identifiants

pubmed: 37798786
doi: 10.1186/s13075-023-03142-3
pii: 10.1186/s13075-023-03142-3
pmc: PMC10552372
doi:

Substances chimiques

Core Binding Factor Alpha 1 Subunit 0
Cytokines 0
GRB2 Adaptor Protein 0
GRB2 protein, human 0
Proto-Oncogene Proteins c-sis 0
RUNX2 protein, human 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

194

Informations de copyright

© 2023. BioMed Central Ltd., part of Springer Nature.

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Auteurs

Yulong Tang (Y)

State Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.

Kai Yang (K)

Department of Dermatology, Jing'an District Central Hospital, Shanghai, China.
Division of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.

Qingmei Liu (Q)

Division of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.

Yanyun Ma (Y)

State Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.

Hao Zhu (H)

Stem Cell Base, Shanghai East Hospital, Shanghai, China.

Kunhai Tang (K)

State Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.

Chengchun Geng (C)

State Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.

Jiangnan Xie (J)

State Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.

Dachun Zhuo (D)

State Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.

Wenyu Wu (W)

Department of Dermatology, Jing'an District Central Hospital, Shanghai, China.
Division of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.

Li Jin (L)

State Key Laboratory of Genetic Engineering, School of Life Science, and Human Phenome Institute, Zhangjiang Fudan International Innovation Center, Fudan University, Shanghai, China.

Wenze Xiao (W)

Department of Rheumatology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, China. wenzexiao@fudan.edu.cn.

Jiucun Wang (J)

State 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.
Research Unit of Dissecting the Population Genetics and Developing New Technologies for Treatment and Prevention of Skin Phenotypes and Dermatological Diseases (2019RU058), Chinese Academy of Medical Sciences, Shanghai, China. jcwang@fudan.edu.cn.

Qi Zhu (Q)

Institute of Arthritis Research, Shanghai Academy of Chinese Medical Sciences, Guanghua Integrative Medicine Hospital, Shanghai, China. zhuqigh540@126.com.
Arthritis Institute of Integrated Traditional and Western Medicine, Shanghai Chinese Medicine Research Institute, Shanghai, China. zhuqigh540@126.com.

Jing Liu (J)

State 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.

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