中华风湿病学杂志
中華風濕病學雜誌
중화풍습병학잡지
Chinese Journal of Rheumatology
2015年
10期
652-655,封3
,共5页
孙琳%李常虹%武东%邢瑞%杨麟%刘蕊%赵金霞%刘湘源
孫琳%李常虹%武東%邢瑞%楊麟%劉蕊%趙金霞%劉湘源
손림%리상홍%무동%형서%양린%류예%조금하%류상원
关节炎,类风湿%间质干细胞%半乳糖凝集素1
關節炎,類風濕%間質榦細胞%半乳糖凝集素1
관절염,류풍습%간질간세포%반유당응집소1
Arthritis,rheumatoid%Mesenchymal stem cells%Galectin 1
目的 明确半乳糖凝集素-1 (galectin-1)在脐带间充质干细胞(UC-MSCs)调控RA成纤维样滑膜细胞(FES)功能中的作用.方法 用慢病毒构建galectin-1低表达的UC-MSCs,即UC-MSCs(Gal-1-).采用Transwell非细胞接触方式分别将UC-MSCs及UC-MSCs(Gal-1-)和FLSs共培养.MTS法检测FLSs增殖,将基质胶铺在Transwell板中来检测UC-MSCs(Gal-1-)对FLSs侵袭能力的影响.多组间计量资料采用单因素方差分析.结果 UC-MSCs及UC-MSCs(对照shRNA)-FLSs共培养组可明显抑制TNF-α诱导的FLSs的增殖作用,而UC-MSCs(Gal-1-)对此增殖无明显抑制作用.UC-MSCs及UC-MSCs(对照shRNA)可显著抑制TNF-α引起的FLSs侵袭细胞数(37±7,42±10与55±14,F=23.50,P<0.05),但UC-MSCs(Gal-1-)-TNF组与TNF-α刺激组相比,侵袭细胞数差异无统计学意义(46±11,P>0.05).结论 UC-MSCs可抑制RA患者FLS的增殖及侵蚀能力,但敲低galectin-1分子的表达后该作用减弱,提示galectin-1参与了UC-MSCs抑制FLS功能的过程.
目的 明確半乳糖凝集素-1 (galectin-1)在臍帶間充質榦細胞(UC-MSCs)調控RA成纖維樣滑膜細胞(FES)功能中的作用.方法 用慢病毒構建galectin-1低錶達的UC-MSCs,即UC-MSCs(Gal-1-).採用Transwell非細胞接觸方式分彆將UC-MSCs及UC-MSCs(Gal-1-)和FLSs共培養.MTS法檢測FLSs增殖,將基質膠鋪在Transwell闆中來檢測UC-MSCs(Gal-1-)對FLSs侵襲能力的影響.多組間計量資料採用單因素方差分析.結果 UC-MSCs及UC-MSCs(對照shRNA)-FLSs共培養組可明顯抑製TNF-α誘導的FLSs的增殖作用,而UC-MSCs(Gal-1-)對此增殖無明顯抑製作用.UC-MSCs及UC-MSCs(對照shRNA)可顯著抑製TNF-α引起的FLSs侵襲細胞數(37±7,42±10與55±14,F=23.50,P<0.05),但UC-MSCs(Gal-1-)-TNF組與TNF-α刺激組相比,侵襲細胞數差異無統計學意義(46±11,P>0.05).結論 UC-MSCs可抑製RA患者FLS的增殖及侵蝕能力,但敲低galectin-1分子的錶達後該作用減弱,提示galectin-1參與瞭UC-MSCs抑製FLS功能的過程.
목적 명학반유당응집소-1 (galectin-1)재제대간충질간세포(UC-MSCs)조공RA성섬유양활막세포(FES)공능중적작용.방법 용만병독구건galectin-1저표체적UC-MSCs,즉UC-MSCs(Gal-1-).채용Transwell비세포접촉방식분별장UC-MSCs급UC-MSCs(Gal-1-)화FLSs공배양.MTS법검측FLSs증식,장기질효포재Transwell판중래검측UC-MSCs(Gal-1-)대FLSs침습능력적영향.다조간계량자료채용단인소방차분석.결과 UC-MSCs급UC-MSCs(대조shRNA)-FLSs공배양조가명현억제TNF-α유도적FLSs적증식작용,이UC-MSCs(Gal-1-)대차증식무명현억제작용.UC-MSCs급UC-MSCs(대조shRNA)가현저억제TNF-α인기적FLSs침습세포수(37±7,42±10여55±14,F=23.50,P<0.05),단UC-MSCs(Gal-1-)-TNF조여TNF-α자격조상비,침습세포수차이무통계학의의(46±11,P>0.05).결론 UC-MSCs가억제RA환자FLS적증식급침식능력,단고저galectin-1분자적표체후해작용감약,제시galectin-1삼여료UC-MSCs억제FLS공능적과정.
Objective To investigate the effects of galectin-1 on regulating of umbilical cord mesenchymal stem cells (UC-MSCs) of rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLSs).Methods Lentivirus transfected shRNA technique was used to knock down the expression of galectin-1 in UC-MSCs to construct UC-MSCs (Gal-1-).The effects of UC-MSCs and UC-MSCs (Gal-1-) on FLSs in RA patients were investigated by transwell system.The proliferation of FLSs was detected by MTS assay.The effect of UC-MSCs on the invasion of FLSs was detected by matrix gel in transell plate.Measurement data were analyzed with oneway analysis of variance.Results In vitro, UC-MSCs were capable of inhibiting tumour necrosis factor-α(TNF-α) induced proliferation of FLSs from RA patients, but UC-MSCs (Gal-1-) did not show significant inhibitory effect.Furthermore, the invasive behavior of FLSs was also significantly suppressed by UC-MSCs (37±7, 42±10, 55±4, F=23.50, P<0.05).These was no significant difference in the number of invasive cells between TNF-α group and UC-MSCs (Gal-1-)-TNF-α group.Conclusion UC-MSCs can inhibit the proliferation and invasive behavior of FLSs from RA patients, but these effects decline after knocking down the expression of galectin-1.Galectin-1 may take part in the regulation of UC-MSCs on rheumatoid arthritis FLSs.