长链非编码核仁小分子RNA宿主基因1对类风湿关节炎成纤维样滑膜细胞增殖的影响

Effects of small nucleolar Ribonuclei Acid host gene 1 on the proliferation of fibroblastlike synoviocytes in rheumatoid arthritis

目的 初步探讨长链非编码核仁小分子RNA宿主基因1(SNHG1)对RA-成纤维样滑膜细胞(FLS)增殖的影响及可能的机制.方法 组织块培养法培养RA和创伤患者FLS,用实时荧光定量PCR(qPCR)法检测二者SNHG1的表达情况;在RA-FLS中,用小干扰RNA(siRNA)沉默SNHG1表达后,CCK-8法检测细胞增殖活力,流式细胞术检测细胞周期分布,蛋白质印迹法检测周期蛋白(cyclin)D1的表达情况;2组样本比较用独立样本t检验,多组样本间比较采用单因素方差分析.结果 与创伤患者FLS相比,RA-FLS中SNHG1表达上调[(2.13±0.55)与(1.00±0.01)](t=-5.87,P=0.004);在RA-FLS中,沉默SNHG1表达后,与阴性对照相比,SNHG1-siRNA处理组细胞增殖活力下调[(0.930±0.033)与(0.759±0.027)](t=6.879,P=0.002),G2/M+S期细胞所占比例下调[(28.2±1.5)%与(9.7±2.6)%](t=10.715,P<0.01),cyclinD1蛋白表达下调(t=6.168,P=0.004).结论 RA患者滑膜细胞中SNHG1的表达增高,SNHG1可能通过影响cyclinD1蛋白表达参与FLS增殖调控,从而促进滑膜增生.

Objective To preliminary study the effects of long noncoding Ribonuclei Acid(RNA)small nucleolar RNA host gene 1(SNHG1)on proliferation of rheumatoid arthritis(RA)fibroblast-like synoviocytes(FLS)and the possible mechanism.Methods The FLS from RA and trauma group were primarily cultured by the explant culture,and the expression of SNHG1 were detected by quantitative polymerase chain reaction(qPCR).Transfection of siRNA was used to interfere the expression of SNHG1.Cell viability was measured using CCK-8 assay and cell cycle distribution was detected by flow cytometry.And the protein level of cyclinD1 was detected by Western blotting.Independent sample t test was used for the comparison between two groups,and the one-way analysis of variance(ANOVA)analysis was used to compare the samples of multiple groups.Results Compared with FLS from trauma group,SNHG1 expression in RA-FLS was up-regulated[(2.13±0.55)vs(1.00±0.01)](t=-5.87,P=0.004).In RA-FLS,after silencing the expression of SNHG1,the cell viability of SNHG1-siRNA treatment group was down-regulated[(0.930±0.033)vs(0.759±0.027)](t=6.879,P=0.002),the proportion of G2/M+S cells was down-regulated[(28.2±1.5)%vs(9.7±2.6)%](t=10.715,P<0.01),and thelevelof cyclinD1 protein was down-regulated(t=6.168,P=0.004)compared with the negative control group.Conclusion The SNHG1 is abnormally expressed in RA-FLS,and SNHG1 may participate in the regulation of FLS proliferation by affecting the expression of cyclinD1 protein,thereby contributing to synovial hyperplasia.