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作 者:杨澜波 邹春雨[1] 米豫飞[1] 黄涛[2] 王战朝[1] Yang Lanbo;Zou Chunyu;Mi Yufei(Luoyang Orthopedic-traumatological Hospital of Henan Province,Henan 471002,China)
机构地区:[1]河南省洛阳正骨医院、河南省骨科医院,471002 [2]中国人民解放军联勤保障部队第989医院,洛阳471031
出 处:《医学研究杂志》2021年第12期89-93,共5页Journal of Medical Research
基 金:河南省中医药科学研究专项基金资助项目(20-21ZY2230)。
摘 要:目的了解USP49对IL-1β诱导的软骨细胞凋亡及细胞外基质降解的影响。方法首先基于数据库了解USP49在骨关节炎患者中的表达水平。原代培养软骨细胞并鉴定,使用不同浓度的IL-1β预处理软骨细胞,检测USP49基因表达与蛋白水平后,选择合适的IL-1β浓度模拟骨关节炎。使用IL-1β处理构建的USP49过表达软骨细胞,检测软骨细胞凋亡,测定USP49、β-catenin及软骨降解相关蛋白MMP-1、MMP-13表达。结果较正常人样本,USP49在骨性关节炎患者中表达显著降低。原代软骨细胞经不同浓度IL-1β预处理后,USP49表达明显抑制,且随浓度增加,抑制作用增强。USP49过表达可显著减弱IL-1β诱导的细胞凋亡,抑制β-catenin、MMP-1、MMP-13表达。结论USP49可能通过Wnt/β-catenin通路抑制软骨细胞凋亡及细胞外基质降解,减轻IL-1β诱导的软骨退变。Objective To investigate the effect of USP49 on chondrocyte apoptosis and expression of proteins related to cartilage metabolism induced by IL-1β.Methods The expression of USP49 in osteoarthritis patients was determined based on GSE57218 database.Primary Rat articular chondrocytes were cultured and identified.After being pretreated with different concentrations of IL-1βrespectively,USP49 gene expression was detected to selecting appropriate IL-1βconcentration for simulating osteoarthritis.After incubation with 10ng/ml IL-1β,the apoptosis of constructed USP49 overexpressed chondrocyte and the expression ofβ-catenin,proteins related to cartilage degradation were detected.Results The expression of USP49 was significantly decreased in patients with osteoarthritis.RT-PCR and Western blot showed that IL-1βsignificantly inhibited USP49 expression in a concentration-dependent manner.Over-expressioned USP49 significantly attenuated the apoptosis of chondrocytes induced by IL-1β,inhibited Wnt/β-catenin pathway and the expression of proteins related to cartilage degradation.Conclusion USP49 inhibits chondrocyte apoptosis and alleviates cartilage degradation induced by IL-1βthrough Wnt/β-catenin pathway.
关 键 词:软骨退行性改变 泛素特异性蛋白酶49 WNT/Β-CATENIN通路
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