摘要
目的:探讨重症肌无力(MG)患者胸腺miRNAs的表达及相关作用机制,为临床诊疗提供理论和实验依据。方法:采用miRNA芯片技术分析MG患者差异miRNA表达并进行功能聚类分析;采用荧光定量PCR和原位杂交荧光技术验证miR-19a-3p在胸腺组织的表达;采用miR-19a-3p mimics转染TALL-104细胞系,观察miR-19a-3p对细胞增殖、凋亡及相关分子(BCL2、SOCS3)表达的影响。结果:与正常胸腺组织相比,MG患者胸腺组织中282个miRNAs的表达具有差异,其中103个上调,179个下调,这些差异miRNAs的主要功能靶基因是细胞核内分子、胞浆中膜样结构及细胞器相关分子。荧光定量PCR和原位荧光杂交证实miR-19a-3p在MG患者胸腺表达显著低于对照组正常胸腺;与对照组相比,miR-19a-3p mimics转染能显著抑制TALL-104细胞凋亡,BCL2表达升高,SOCS3表达降低(P<0.05)。结论:MG患者胸腺miRNA表达与非MG患者胸腺相比差异有统计学意义,其中miR-19a-3p通过上调BCL2以及下调SOCS3抑制T细胞凋亡。
Objective:To investigate the expression of miRNAs in thymus of patients with myasthenia gravis(MG)and the re-lated mechanism of action,so as to provide theoretical and experimental basis for clinical diagnosis and treatment.Methods:miRNA microarray technology was used to analyze the differential miRNA expression in MG patients thymus.Fluorescence quantitative PCR and in situ hybridization were used to verify the expression of miR-19a-3p in thymus tissue.The TALL-104 cell line was transfected with miR-19a-3p mimics to observe the effects of miR-19a-3p on cell proliferation,apoptosis and expressions of related molecules(BCL2 and SOCS3).Results:Compared to normal thymus tissue,a total of 282 differentially expressed miRNAs were detected in the thymus of MG patients,among which 103 were up-regulated and 179 were down-regulated.The target genes of differentially expressed miRNAs were mainly related to nuclear molecules,cytoplasmic membrane-like structures and organelle related molecules.Quantita-tive fluorescence PCR and in situ fluorescence hybridization confirmed that the expression of miR-19a-3p in MG patients thymus was significantly lower than that in normal control group.Compared with the control group,miR-19a-3p mimics transfection could signifi-cantly inhibit the apoptosis of TALL-104 cells,increase the expression of BCL2 and decrease the expression of SOCS3(P<0.05).Conclusion:The expression of miRNA in the thymus of MG patients is significantly different from that of non-MG patients,and miR-19a-3p inhibits T cell apoptosis through up-regulation of BCL2 and down-regulation of SOCS3.
作者
孙蕾
赵瑞
李倩如
轩小燕
王鹏
杜英
刘萍萍
SUN Lei;ZHAO Rui;LI Qianru;XUAN Xiaoyan;WANG Peng;DU Ying;LIU Pingping(Physical Examination Center,the First Affiliated Hospital of Henan University of CM,Zhengzhou 450000,China;Department of Laboratory Science,the Third Affiliated Hospital of Zhengzhou University,Zhengzhou 450052,China;Department of Microbiology and Immunology,School of Basic Medicine,Zhengzhou University,Zhengzhou 450001,China)
出处
《中国免疫学杂志》
北大核心
2025年第8期1980-1984,共5页
Chinese Journal of Immunology
基金
国家自然科学基金(81471545)。
