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(FLS)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。
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-a (TNF-a) 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 (37e7, 42±10, 55±4, F=23.50, P〈0.05). These was no significant difference in the number of invasive cells between TNF-ot group and UC-MSCs (Gal-1-)-TNF-ot 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.