向FGFR3是一种有用的治疗策略,用于治疗类风湿性关节炎
Shan-Fu Yu1,2,3, Tien-Tsai Cheng1,3, Gong-Kai Huang4
1Division of Rheumatology, Allergy, and Immunology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Current molecular pharmacology
|November 20, 2023
概括
纤维细胞生长因子受体3 (FGFR3) 在类风湿性关节炎 (RA) 突细胞中被上调. 抑制FGFR3会减少细胞增殖,迁移和炎症,这表明FGFR3是RA的治疗点.
科学领域:
- 类风湿病学 类风湿病学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 类风湿性关节炎 (RA) 是一种全身性炎症性疾病.
- 瘤坏死因子-α (TNF-α) 在RA的发病过程中起着关键作用.
- 纤维细胞生长因子受体3 (FGFR3) 通过调节炎性细胞因子表达,与RA有关.
研究的目的:
- 为了研究FGFR3表达在人类RA突组织.
- 评估FGFR3基因沉默对突细胞行为的影响.
主要方法:
- 在人类RA关节组织中对FGFR3进行免疫组织化学染色.
- 细胞增殖,迁移和细胞亡测定在SW-982细胞与FGFR3siRNA.
- 免疫光和西式涂抹检测分子变化.
主要成果:
- 在RA患者的细胞质和突细胞核中,FGFR3被上调.
- 抑制FGFR3降低了突细胞的增殖和迁移,并诱导了亡.
- 抑制FGFR3降低了TNF-α,NF-κB,COX-2,MMP-9和上皮-介质细胞转变 (EMT) 标记物的表达,同时增加了E-cadherin.
结论:
- 基因干扰的FGFR3调节的炎症介质和EMT标记在突细胞.
- 针对FGFR3/MAPK信号通路为RA发展提供了潜在的治疗策略.
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