The effect of kynurenine-3-monooxygenase on the function of fibroblast-like synoviocytes in rheumatoid arthritis
10.19405/j.cnki.issn1000-1492.2026.08.010
- VernacularTitle:犬尿氨酸-3-单加氧酶对类风湿关节炎成纤维样滑膜细胞功能的影响
- Author:
Yongping JIA
1
;
Xuemei ZONG
1
;
Yannan WANG
1
;
Wenli WANG
1
;
Yueye WANG
1
;
Wei WEI
1
;
Yan CHANG
1
Author Information
1. Institute of Clinical Pharmacology， School of Pharmacy， Anhui Medical University， Key Laboratory of Anti-inflammatory and Immune Medicine， Ministry of Education， Hefei 230032
- Publication Type:Journal Article
- Keywords:
rheumatoid arthritis;
kynurenine-3-monooxygenase;
fibroblast-like synoviocytes;
proliferation;
migration;
secretion
- From:
Acta Universitatis Medicinalis Anhui
2026;61(8):1408-1415
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effect of kynurenine-3-monooxygenase （KMO） on the function of fibroblast-like synoviocytes （FLS） in rheumatoid arthritis （RA）. MethodsKMO expression in synovial tissues from RA patients and healthy controls （HC） was analyzed using bioinformatics. Synovial tissues from RA patients and HC were collected， and KMO expression in FLS within synovial tissues was detected by immunofluorescence （IF）. In vitro experiments were performed using human rheumatoid arthritis fibroblast-like synoviocytes （MH7A）. Following KMO overexpression， KMO knockdown， and KMO inhibition with the specific inhibitor Ro61-8048 in MH7A cells， Western blot， CCK-8， EdU， Transwell and ELISA assays were used to evaluate alterations in cell viability， proliferation， migration and secretory function. ResultsBioinformatic analysis revealed significantly higher KMO gene expression in RA synovial tissue compared to the HC group （P<0.001）. IF results showed increased KMO expression in FLS from RA synovial tissues relative to the HC group （P<0.01）. Overexpression of KMO led to enhanced viability， proliferation， migration， and secretory capabilities of MH7A cells （all P<0.05）， whereas knockdown or inhibition of KMO with Ro61-8048 markedly suppressed these functions （all P<0.05）. ConclusionThe expression of KMO is upregulated in the synovial tissues of RA patients and promotes the activation of RA-FLS， suggesting that KMO may serve as a potential therapeutic target for RA treatment.
