Interleukin-17A promotes osteoclastogenesis in chronic gouty arthritis
10.16352/j.issn.1001-6325.2025.12.1608
- VernacularTitle:IL-17A促进慢性痛风性关节炎中破骨细胞形成
- Author:
Yibo WANG
1
;
Hong DI
;
Xiaohan ZHANG
;
Yun ZHANG
;
Xuejun ZENG
Author Information
1. 中国医学科学院 北京协和医学院 北京协和医院 全科医学科(普通内科),北京 100730
- Keywords:
gout;
IL-17A;
osteoclast;
mitophagy;
bone erosion
- From:
Basic & Clinical Medicine
2025;45(12):1608-1613
- CountryChina
- Language:Chinese
-
Abstract:
Objective Chronic gouty arthritis(CGA)can lead to severe bone erosion resulting in joint destruction,which significantly decreases the life quality and prognosis of CGA patients.Osteoclasts play an important role in this course.We aim to investigate the effect of interleukin-17A(IL-17A)on osteoclast formation in vitro in patients with chronic gouty arthritis(CGA)and its potential mechanism.Methods Osteoclasts induced in vitro from pe-ripheral blood mononuclear cells(PBMC)of healthy controls(HC)and CGA patients were studied.CGA-derived osteoclasts were divided into four groups:untreated group,IL-17A-treated group,carbonyl cyanide 3-chlorophenyl-hydrazone(CCCP)group,and mitochondrial division inhibitor-1(Mdivi-1)group.Tartrate-resistant acid phospha-tase(TRAP)staining was used to observe and compare osteoclastogenesis between HC and the untreated group.Western blot was performed to detect mitophagy levels and the expression of key osteoclast differentiation factors.Results Compared with healthy controls,CGA patients showed higher osteoclastogenesis(P＜0.01).Compared with the untreated group,the IL-17A-treated group showed up-regulated expression of key osteoclast transcription factors and decreased mitophagy levels(P＜0.05).Intervention with 10 nmol/L and 15 nmol/L Mdivi-1 significantly promoted the expression of key osteoclast transcription factors(P＜0.01).Conclusions IL-17A promotes osteoclast formation in vitro in CGA patients,and its mechanism may be related to decreased mitophagy levels.
